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Publications of Amir H. Rezvani    :chronological  alphabetical  combined listing:

%% Journal Articles   
@article{fds275603,
   Author = {Rezvani, AH and Sexton, HG and Levin, ED},
   Title = {ASSESSMENT OF PREGNENOLONE EFFECTS ON ALCOHOL INTAKE IN MALE
             ALCOHOL PREFERRING RATS},
   Journal = {Alcoholism, Clinical and Experimental Research},
   Volume = {36},
   Pages = {101A-101A},
   Year = {2012},
   Month = {June},
   ISSN = {0145-6008},
   url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000304806000362&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=47d3190e77e5a3a53558812f597b0b92},
   Key = {fds275603}
}


%% Papers Published   
@article{fds339904,
   Author = {DiPalma, D and Rezvani, AH and Willette, B and Wells, C and Slade, S and Hall, BJ and Levin, ED},
   Title = {Persistent attenuation of nicotine self-administration in
             rats by co-administration of chronic nicotine infusion with
             the dopamine D1 receptor antagonist SCH-23390 or the
             serotonin 5-HT2C agonist lorcaserin.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {176},
   Pages = {16-22},
   Year = {2018},
   Month = {November},
   url = {http://dx.doi.org/10.1016/j.pbb.2018.11.002},
   Abstract = {Tobacco addiction each year causes millions of deaths
             worldwide. Brain nicotinic acetylcholine receptors have been
             shown to be central to tobacco addiction. Nicotine
             replacement therapy aids tobacco cessation, but the success
             rate is still far too low. This may in part be due to the
             fact that neurons with nicotinic receptors are not the only
             neural systems involved in tobacco addiction. Interacting
             neural systems also play important roles in tobacco
             addiction. Nicotine increases the release of a variety of
             neurotransmitters, including dopamine and serotonin.
             Dopamine, in particular dopamine D1 receptors, has been
             shown to be involved in the reinforcing action of nicotine.
             Serotonin through its actions on 5-HT2C receptors has been
             shown to play a key role in modulating the reinforcement of
             addictive drugs, including nicotine and alcohol. Combination
             of treatments could provide greater treatment efficacy.
             These studies were conducted to evaluate combination
             therapies utilizing nicotine replacement therapy in
             conjunction with either a dopamine D1 receptor antagonist
             SCH-23390 or a serotonin 5-HT2C receptor agonist,
             lorcaserin. Female Sprague-Dawley rats were given access to
             self-administer nicotine via IV infusions. Osmotic pumps
             were implanted to reproduce the kinetic of chronic nicotine
             patch therapy. SCH-23390 (0.02 mg/kg) or lorcaserin
             (0.6 mg/kg) were administered prior to nicotine
             self-administration sessions. Reproducing earlier findings
             SCH-23390, lorcaserin and nicotine replacement therapy were
             effective at reducing IV nicotine self-administration. 5HT2C
             agonist treatment had additive effects with chronic nicotine
             infusion for significantly lowering nicotine
             self-administration. This study demonstrates the feasibility
             of combination of chronic nicotine with therapies targeting
             non-nicotinic receptors as treatment options for tobacco
             addiction.},
   Doi = {10.1016/j.pbb.2018.11.002},
   Key = {fds339904}
}

@article{fds332662,
   Author = {Levin, ED and Wells, C and Slade, S and Rezvani, AH},
   Title = {Mutually augmenting interactions of dextromethorphan and
             sazetidine-A for reducing nicotine self-administration in
             rats.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {166},
   Pages = {42-47},
   Year = {2018},
   Month = {March},
   url = {http://dx.doi.org/10.1016/j.pbb.2018.01.005},
   Abstract = {A variety of nicotinic drug treatments have been found to
             decrease nicotine self-administration. However, interactions
             of drugs affecting different nicotinic receptor subtypes
             have not been much investigated. This study investigated the
             interactions between dextromethorphan, which blocks
             nicotinic α3β2 receptors as well as a variety of other
             receptors with sazetidine-A which is a potent and selective
             α4β2 nicotinic receptor partial agonist with desensitizing
             properties. This interaction was compared with
             dextromethorphan combination treatment with mecamylamine,
             which is a nonspecific nicotinic channel blocker.
             Co-administration of dextromethorphan (either 0.5 or
             5 mg/kg) and lower dose of sazetidine-A (0.3 mg/kg)
             caused a significant reduction in nicotine SA. With regard
             to food-motivated responding, 3 mg/kg of sazetidine-A
             given alone caused a significant decrease in food intake.
             However, the lower 0.3 mg/kg sazetidine-A dose did not
             significantly affect food-motivated responding even when
             given in combination with the higher 5 mg/kg
             dextromethorphan dose which itself caused a significant
             decrease in food motivated responding. Interestingly, this
             higher dextromethorphan dose significantly attenuated the
             decrease in food motivated responding caused by 3 mg/kg of
             sazetidine-A. Locomotor activity was increased by the lower
             0.3 mg/kg sazetidine-A dose and decreased by the 5 mg/kg
             dextromethorphan dose. Mecamylamine at the doses (0.1 and
             1 mg/kg) did not affect nicotine SA, but at 1 mg/kg
             significantly decreased food-motivated responding. None of
             the mecamylamine doses augmented the effect of
             dextromethorphan in reducing nicotine self-administration.
             These studies showed that the combination of
             dextromethorphan and sazetidine-A had mutually potentiating
             effects, which could provide a better efficacy for promoting
             smoking cessation, however the strength of the interactions
             was fairly modest.},
   Doi = {10.1016/j.pbb.2018.01.005},
   Key = {fds332662}
}

@article{fds332324,
   Author = {Rezvani, AH and Tizabi, Y and Slade, S and Getachew, B and Levin,
             ED},
   Title = {Sub-anesthetic doses of ketamine attenuate nicotine
             self-administration in rats.},
   Journal = {Neuroscience Letters},
   Volume = {668},
   Pages = {98-102},
   Year = {2018},
   Month = {March},
   url = {http://dx.doi.org/10.1016/j.neulet.2018.01.022},
   Abstract = {Smoking cessation strategies are of prime medical
             importance. Despite availability of various pharmacological
             agents in combating addiction to nicotine, more effective
             medications are needed. Based on recent findings, the
             glutamatergic system in the brain may provide novel targets.
             Here, we evaluated the effects of acute administration of
             sub-anesthetic doses of ketamine, an NMDA receptor
             antagonist, in both male and female Sprague-Dawley rats
             trained to self-administer nicotine. Animals were injected
             subcutaneously with 5, 7.5 and 10 mg/kg ketamine or saline
             and the effects on the number of intravenous nicotine
             infusions during a 45 min session was measured. Ketamine
             treatment significantly reduced nicotine self-administration
             in a dose-dependent manner. Moreover, a differential
             sensitivity between the sexes was observed as male rats
             responded to a lower dose of ketamine and with higher
             magnitude of effect than female rats. It is concluded that
             glutamatergic receptor manipulations may offer a novel and
             potentially sex-dependent intervention in nicotine
             addiction.},
   Doi = {10.1016/j.neulet.2018.01.022},
   Key = {fds332324}
}

@article{fds326640,
   Author = {Rezvani, AH and Slade, S and Wells, C and Yenugonda, VM and Liu, Y and Brown, ML and Xiao, Y and Kellar, KJ and Levin, ED},
   Title = {Differential efficacies of the nicotinic α4β2
             desensitizing agents in reducing nicotine
             self-administration in female rats.},
   Journal = {Psychopharmacology},
   Volume = {234},
   Number = {17},
   Pages = {2517-2523},
   Year = {2017},
   Month = {September},
   url = {http://dx.doi.org/10.1007/s00213-017-4641-6},
   Abstract = {Desensitization of neuronal nicotinic acetylcholine
             receptors holds promise as an effective treatment of tobacco
             addiction. Previously, we found that sazetidine-A (Saz-A),
             which selectively desensitizes α4β2 nicotinic receptors,
             significantly decreased intravenous (IV) nicotine
             self-administration (SA) in rats with an effective dose of
             3 mg/kg in acute and repeated injection studies. We also
             found that chronic infusions of Saz-A at doses of 2 and
             6 mg/kg/day significantly reduced nicotine SA in rats. In
             continuing studies, we have characterized other Saz-A
             analogs, YL-2-203 and VMY-2-95, to determine their
             efficacies in reducing nicotine SA in rats.Young adult
             female Sprague-Dawley rats were fitted with IV catheters and
             were trained for nicotine SA (0.03 mg/kg/infusion) on a
             fixed ratio 1 schedule for ten sessions. The same rats were
             also implanted subcutaneously with osmotic minipumps to
             continually deliver 2 or 6 mg/kg body weight YL-2-203,
             VMY-2-95, or saline for four consecutive weeks.Chronic
             administration of VMY-2-95 at doses of 2 and 6 mg/kg/day
             caused significant (p < 0.01) decreases in nicotine SA
             over the 2 weeks of continued nicotine SA and for the
             1-week period of resumed access after a week of enforced
             abstinence, whereas chronic administration of YL-2-203 at
             the same doses was not found to be effective.These studies,
             together with our previous studies of Saz-A, revealed a
             spectrum of efficacies for these α4β2 nicotinic receptor
             desensitizing agents and provide a path forward for the most
             effective compounds to be further developed as possible aids
             to smoking cessation.},
   Doi = {10.1007/s00213-017-4641-6},
   Key = {fds326640}
}

@article{fds328872,
   Author = {Rezvani, AH and Levin, ED and Cauley, M and Getachew, B and Tizabi,
             Y},
   Title = {Ketamine Differentially Attenuates Alcohol Intake in Male
             Versus Female Alcohol Preferring (P) Rats.},
   Journal = {Journal of Drug and Alcohol Research},
   Volume = {6},
   Pages = {1-6},
   Year = {2017},
   Month = {January},
   url = {http://dx.doi.org/10.4303/jdar/236030},
   Abstract = {Although various pharmacological tools in combating
             addiction to alcohol are available, their efficacy is
             limited. Hence, there is a critical need for development of
             more effective medications. Recent advances in the field
             have identified the glutamatergic system as a potential
             novel target for intervention in addictive behaviors.Hence,
             we evaluated the effects of acute administration of low
             (subanesthetic) doses of ketamine, an NMDA receptor
             antagonist, on alcohol intake and alcohol preference in both
             male and female rats.Adult alcohol preferring (P) rats were
             exposed to two-bottle choice (ethanol 10% and water) for at
             least three weeks following a nine-day training period and
             the effects of various doses of ketamine (5 mg/kg, 7.5
             mg/kg, and 10 mg/kg, injected subcutaneously, SC) on
             consumption of alcohol over various time periods during a 24
             h interval were measured.Our results indicate that ketamine
             treatment significantly reduced both alcohol intake and
             preference in a time- and dose-dependent manner in both
             sexes. Moreover, a differential sensitivity between the
             sexes was observed. Thus, although alcohol intake was higher
             in males, female rats responded much more strongly to the
             highest dose of ketamine than males in the initial time
             periods.It is concluded that glutamatergic receptor
             manipulations may be of therapeutic potential in addiction
             to alcohol and that different sexes may respond
             differentially to such treatments.},
   Doi = {10.4303/jdar/236030},
   Key = {fds328872}
}

@article{fds323344,
   Author = {Rezvani, AH and Cauley, MC and Slade, S and Wells, C and Glick, S and Rose,
             JE and Levin, ED},
   Title = {Acute oral 18-methoxycoronaridine (18-MC) decreases both
             alcohol intake and IV nicotine self-administration in
             rats.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {150-151},
   Pages = {153-157},
   Year = {2016},
   Month = {November},
   url = {http://dx.doi.org/10.1016/j.pbb.2016.10.010},
   Abstract = {The ibogaine derivative 18-methoxycoronaridine (18-MC) has
             been found to decrease self-administration of morphine,
             nicotine and alcohol in rats after systemic injection.
             However oral dosing is the preferred route clinically. The
             current study evaluated the effect of oral 18-MC dosing in
             rats on alcohol and nicotine self-administration. For the
             nicotine study, young adult female Sprague-Dawley rats were
             fitted with IV jugular infusion catheters and trained for
             nicotine self-administration in 45min. sessions. At weekly
             intervals they were administered by oral gavage doses of
             18-MC (0, 10, 20 and 40mg/kg) following a repeated measures
             counterbalanced design twice. Acute oral 18-MC, at the
             40mg/kg dosage, significantly reduced nicotine
             self-administration. There was a differential effect of
             18-MC with rats above or below the median level of nicotine
             self-administration during the pretreatment baseline
             performance. Rats with lower baseline performance showed a
             significant reduction in nicotine self-administration with
             the 40mg/kg dosage, while those in the higher baseline group
             did not show a significant effect of 18-MC. In alcohol
             studies, the effects of the same doses of 18-MC were tested
             in both male and female alcohol preferring (P) rats that had
             free access to water and alcohol (10% v/v) 6h/day. The
             results show that 18-MC dose-dependently reduced alcohol
             intake in both male and female rats. All doses caused
             significant reductions in alcohol self-administration. These
             data reinforce previous findings that 18-MC is significantly
             effective in reducing alcohol intake and nicotine
             self-administration. The finding that 18-MC is also
             effective orally makes it advantageous for further
             development as a possible new therapy for treating
             alcoholism as well as smoking addiction.},
   Doi = {10.1016/j.pbb.2016.10.010},
   Key = {fds323344}
}

@article{fds322128,
   Author = {Levin, ED and Hall, BJ and Chattopadhyay, A and Slade, S and Wells, C and Rezvani, AH and Rose, JE},
   Title = {Reduction of nicotine self-administration by chronic
             nicotine infusion with H1 histamine blockade in female
             rats.},
   Journal = {Psychopharmacology},
   Volume = {233},
   Number = {15-16},
   Pages = {3009-3015},
   Year = {2016},
   Month = {August},
   url = {http://dx.doi.org/10.1007/s00213-016-4347-1},
   Abstract = {Chronic nicotine infusion via transdermal patches has been
             widely shown to assist with smoking cessation. In
             particular, transdermal nicotine treatment prior to quitting
             smoking helps reduce ad libitum smoking and aids cessation
             Rose et al. (Nicotine Tob Res 11:1067-75, 2009). However,
             despite this success, the majority of smokers who use
             transdermal nicotine fail to permanently quit smoking.
             Additional treatments are needed. Tobacco addiction does not
             just depend on nicotinic receptor systems; a variety of
             neural systems are involved, including dopamine,
             norepinepherine, serotonin, and histamine.Given the
             involvement of a variety of neural systems in the circuits
             of addiction, combination therapy may offer improved
             efficacy for successful smoking cessation beyond single
             treatments alone. We have found that pyrilamine, an H1
             histamine antagonist, significantly decreases nicotine
             self-administration in rats.The current study was conducted
             to confirm the effect of chronic nicotine infusion on
             ongoing nicotine self-administration and resumed access
             after enforced abstinence and to determine the interaction
             of chronic nicotine with an H1 antagonist treatment.Chronic
             nicotine infusion via osmotic minipump (2.5 and 5 mg/kg/day
             for 28 days) significantly reduced nicotine
             self-administration in a dose-dependent manner. Chronic
             nicotine infusion also reduced the resumption of nicotine
             self-administration after enforced abstinence. Chronic
             pyrilamine infusion (25 mg/kg/day for 14 days) also
             significantly reduced nicotine self-administration.The
             combination of chronic nicotine and pyrilamine reduced
             nicotine self-administration to a greater extent than
             treatment with either drug alone.},
   Doi = {10.1007/s00213-016-4347-1},
   Key = {fds322128}
}

@article{fds322129,
   Author = {Briggs, SA and Hall, BJ and Wells, C and Slade, S and Jaskowski, P and Morrison, M and Rezvani, AH and Rose, JE and Levin,
             ED},
   Title = {Dextromethorphan interactions with histaminergic and
             serotonergic treatments to reduce nicotine
             self-administration in rats.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {142},
   Pages = {1-7},
   Year = {2016},
   Month = {March},
   url = {http://dx.doi.org/10.1016/j.pbb.2015.12.004},
   Abstract = {Combining effective treatments with diverse mechanisms of
             action for smoking cessation may provide better therapy by
             targeting multiple points of control in the neural circuits
             underlying addiction. Previous research in a rat model has
             shown that dextromethorphan, which has α3β4 nicotinic and
             NMDA glutamatergic antagonist actions, significantly
             decreases nicotine self-administration. We have found in the
             rat model that the H1 histamine antagonist pyrilamine and
             the serotonin 5HT2C agonist lorcaserin also significantly
             reduce nicotine self-administration. The current studies
             were conducted to determine the interactive effects of
             dextromethorphan with pyrilamine and lorcaserin on nicotine
             self-administration in rats. Young adult female rats were
             fitted with jugular IV catheters and trained to
             self-administer a nicotine infusion dose of
             0.03-mg/kg/infusion. In an initial dose-effect function
             study of dextromethorphan, we found a monotonic decrease in
             nicotine self-administration over a dose range of 1 to
             30-mg/kg with the lowest effective dose of 3-mg/kg. Then,
             with two separate cohorts of rats, dextromethorphan (0, 3.3,
             and 10-mg/kg) interactions with pyrilamine (0, 4.43, and
             13.3-mg/kg) were investigated as well as interactions with
             lorcaserin (0, 0.3125 and 0.625-mg/kg). In the
             pyrilamine-dextromethorphan interaction study, an acute dose
             of pyrilamine (13.3-mg/kg) as well as an acute dose of
             dextromethorphan caused a significant decrease in nicotine
             self-administration. There were mutually augmenting effects
             of these two drugs. The combination of dextromethorphan
             (10-mg/kg) and pyrilamine (13.3-mg/kg) significantly lowered
             nicotine self-administration relative to either 10-mg/kg of
             dextromethorphan alone (p<0.05) or 13.3-mg/kg of pyrilamine
             alone (p<0.0005). In the lorcaserin-dextromethorphan study,
             an acute dose of lorcaserin (0.312-mg/kg) as well as an
             acute dose of dextromethorphan (10-mg/kg) caused a
             significant decrease in nicotine self-administration
             replicating previous findings. Augmenting interactions were
             observed with dextromethorphan and pyrilamine as well as
             lorcaserin. These findings suggest that combination therapy
             may be more effective smoking cessation treatments than
             monotherapy.},
   Doi = {10.1016/j.pbb.2015.12.004},
   Key = {fds322129}
}

@article{fds322130,
   Author = {Rezvani, AH and Levin, ED and Wells, C and Slade, S and Morrison, M and Marshall, L and Morris, M and Confino, J and Allenby, C and Lumeng,
             L},
   Title = {Different lines of rats selectively-bred for high
             alcohol-drinking demonstrate disparate preferences for
             nicotine self-administration},
   Journal = {Journal of Drug and Alcohol Research},
   Volume = {2016},
   Number = {5},
   Pages = {1-9},
   Publisher = {Ashdin Publishing},
   Year = {2016},
   Month = {January},
   url = {http://dx.doi.org/10.4303/jdar/235972},
   Abstract = {© 2016 Amir H. Rezvani et al. Background. Alcohol and
             nicotine are commonly coabused. The search for a common core
             of neural, behavioral, and genetic factors underlying
             addiction has been the goal of addiction research. Purpose.
             Genetic predisposition to high alcohol intake has been
             studied in rats by selectively breeding rats that have high
             preference for alcohol. The current experiments were
             conducted to determine if the level of intravenous nicotine
             administration for the various lines of alcohol-preferring
             rats differs from that for nonalcohol-preferring controls.
             Study design. Adult alcohol-naïve selectively-bred
             alcohol-preferring male rats from four lines (P, AA, HAD-1,
             sP) and their control nonalcohol-preferring rats (NP, ANA,
             LAD-1, sNP) were trained and given access to self-administer
             nicotine (0.03mg/kg/infusion). Results. The results show
             that the P rats selfadministered significantly more nicotine
             than NP rats. In contrast, there were no significant
             differences in nicotine self-administration between the sP
             and sNP or the AA and ANA rats. Unexpectedly, high
             alcohol-drinking HAD-1 rats self-administered significantly
             less nicotine than low alcohol-drinking LAD-1 rats.
             Conclusion. This suggests that some genetic factors that
             underlie high-alcohol intake have more general effects in
             promoting high nicotine intake tendencies, while other
             genetic factors are more specific to only heavy
             drinking.},
   Doi = {10.4303/jdar/235972},
   Key = {fds322130}
}

@article{fds323726,
   Author = {Rezvani, AH and Levin, ED and Arolfo, MP and Wells, C and Graupe, M and Diamond, I},
   Title = {Inhibition of Aldehyde Dehydrogenase-2 (ALDH-2) Suppresses
             Nicotine Self-Administration in Rats},
   Journal = {Journal of Drug and Alcohol Research},
   Volume = {4},
   Pages = {1-6},
   Publisher = {Ashdin Publishing},
   Year = {2016},
   url = {http://dx.doi.org/10.4303/jdar/235940},
   Doi = {10.4303/jdar/235940},
   Key = {fds323726}
}

@article{fds291333,
   Author = {Blanchard, H and Chang, L and Rezvani, AH and Rapoport, SI and Taha,
             AY},
   Title = {Brain Arachidonic Acid Incorporation and Turnover are not
             Altered in the Flinders Sensitive Line Rat Model of Human
             Depression.},
   Journal = {Neurochemical Research},
   Volume = {40},
   Number = {11},
   Pages = {2293-2303},
   Year = {2015},
   Month = {November},
   ISSN = {0364-3190},
   url = {http://dx.doi.org/10.1007/s11064-015-1719-6},
   Abstract = {Brain serotonergic signaling is coupled to arachidonic acid
             (AA)-releasing calcium-dependent phospholipase A2. Increased
             brain serotonin concentrations and disturbed serotonergic
             neurotransmission have been reported in the Flinders
             Sensitive Line (FSL) rat model of depression, suggesting
             that brain AA metabolism may be elevated. To test this
             hypothesis, (14)C-AA was intravenously infused to
             steady-state levels into control and FSL rats derived from
             the same Sprague-Dawley background strain, and labeled and
             unlabeled brain phospholipid and plasma fatty acid
             concentrations were measured to determine the rate of brain
             AA incorporation and turnover. Brain AA incorporation and
             turnover did not differ significantly between controls and
             FSL rats. Compared to controls, plasma unesterified
             docosahexaenoic acid was increased, and brain
             phosphatidylinositol AA and total lipid linoleic acid and
             n-3 and n-6 docosapentaenoic acid were significantly
             decreased in FSL rats. Several plasma esterified fatty acids
             differed significantly from controls. In summary, brain AA
             metabolism did not change in FSL rats despite reported
             increased levels of serotonin concentrations, suggesting
             possible post-synaptic dampening of serotonergic
             neurotransmission involving AA.},
   Doi = {10.1007/s11064-015-1719-6},
   Key = {fds291333}
}

@article{fds275589,
   Author = {Levin, ED and Wells, C and Johnson, JE and Rezvani, AH and Bymaster, FP and Rose, JE},
   Title = {Amitifadine, a triple monoamine re-uptake inhibitor, reduces
             nicotine self-administration in female rats.},
   Journal = {European Journal of Pharmacology},
   Volume = {764},
   Pages = {30-37},
   Year = {2015},
   Month = {October},
   ISSN = {0014-2999},
   url = {http://dx.doi.org/10.1016/j.ejphar.2015.06.041},
   Abstract = {A wider diversity of drug treatments to aid smoking
             cessation is needed to help tailor the most efficacious
             treatment for different types of smokers. This study was
             conducted to determine whether amitifadine, which inhibits
             re-uptake of dopamine, norepinephrine and serotonin, would
             decrease nicotine self-administration at doses that do not
             cause adverse side effects. Adult female Sprague-Dawley rats
             were trained to self-administer nicotine intravenous (IV)
             and were given acute doses of amitifadine in a repeated
             measures counterbalanced design. Effects of amitifadine on
             locomotor activity and food motivated responding were also
             evaluated. Chronic amitifadine effects were also examined.
             The 30 mg/kg amitifadine dose significantly reduced nicotine
             self-administration. The 5 and 10 mg/kg doses reduced
             nicotine self-administration during the first 15 min of the
             session when the greatest amount of nicotine was
             self-administered. The 30 mg/kg amitifadine dose, but not
             the lower doses caused a significant reduction in locomotor
             activity averaged over the one-hour session and reduced food
             motivated responding. The 10 mg/kg dose caused hypoactivity
             at the beginning of the session, but 5 mg/kg did not cause
             any hypoactivity. The effects of chronic amitifadine
             treatment (10 mg/kg) over the course of 15 sessions was also
             determined. Amitifadine caused a significant reduction in
             nicotine self-administration, which was not seen to diminish
             over two consecutive weeks of treatment and a week after
             enforced abstinence. Amitifadine significantly reduced
             nicotine self-administration. This prompts further research
             to determine if amitifadine might be an effective treatment
             for smoking cessation.},
   Doi = {10.1016/j.ejphar.2015.06.041},
   Key = {fds275589}
}

@article{fds275590,
   Author = {Levin, ED and Hall, BJ and Rezvani, AH},
   Title = {Heterogeneity across brain regions and neurotransmitter
             interactions with nicotinic effects on memory
             function.},
   Journal = {Current Topics in Behavioral Neurosciences},
   Volume = {23},
   Pages = {87-101},
   Year = {2015},
   Month = {January},
   ISSN = {1866-3370},
   url = {http://dx.doi.org/10.1007/978-3-319-13665-3_4},
   Abstract = {Nicotinic acetylcholine receptors have been shown in many
             studies to be critically involved in memory function. The
             precise roles these receptors play depend on the receptor
             subtype, their anatomic localization, their interactions
             with other parts of the neural systems underlying cognition
             and the particular domain of cognitive function. Nicotinic
             agonists can significantly improve learning, memory, and
             attention. Nicotinic receptors in the hippocampus are
             innervated by cholinergic projections from the medial septum
             and diagonal band. Local infusions of either α7 or α4β2
             nicotinic antagonists into either the dorsal or ventral
             hippocampus produce amnestic effects in rats navigating
             about a radial arm maze. There is cholinergic innervation of
             nicotinic receptors in other components of the limbic system
             as well. In the basolateral amygdala and the anterior
             thalamus, similar amnestic effects of nicotinic α7 and
             α4β2 antagonists are seen. Interestingly, there are no
             additive amnestic effects observed in these limbic areas
             when α7 and α4β2 receptor antagonists are combined. The
             particular expression patterns of α7 and α4β2 nicotinic
             receptors in these limbic and cortical areas may explain
             this nonadditivity, but further research is needed to
             determine the specific cause of this phenomenon. Nicotinic
             receptor mechanisms in the limbic system play an important
             role in cognitive impairment for a variety of neurological
             disorders, including Alzheimer's disease and schizophrenia.
             Alzheimer's disease results in a dramatic decrease in
             hippocampal nicotinic receptor density, affecting α4β2
             receptor expression most prominently. In schizophrenia,
             there are anomalies in α7 nicotinic receptor expression,
             which seem to be crucial for the cognitive impairment of the
             disorder. Chronic nicotine exposure, such as seen with
             tobacco use, results in an increase in nicotinic receptor
             density in the limbic system. This effect appears to be
             related to the desensitization of nicotinic receptors seen
             after agonist application. Open questions remain concerning
             the role of desensitization versus activation of nicotinic
             receptors in cognitive improvement.},
   Doi = {10.1007/978-3-319-13665-3_4},
   Key = {fds275590}
}

@article{fds275591,
   Author = {Rezvani, AH and Cauley, MC and Levin, ED},
   Title = {Lorcaserin, a selective 5-HT(2C) receptor agonist, decreases
             alcohol intake in female alcohol preferring
             rats.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {125},
   Pages = {8-14},
   Year = {2014},
   Month = {October},
   ISSN = {0091-3057},
   url = {http://dx.doi.org/10.1016/j.pbb.2014.07.017},
   Abstract = {Serotonergic systems in the brain have been found to be
             important in the addiction to alcohol. The purpose of this
             study was to evaluate the efficacy of a novel 5-HT2c
             receptor agonist, lorcaserin for reducing alcohol
             consumption in alcohol-preferring (P) rats. Adult female
             rats were allowed to drink water or alcohol (12%, v/v) using
             a standard two-bottle choice procedure. Once stable
             baselines were established, the acute (0, 0.3125, 0.625 and
             1.25 mg/kg, s.c.), and chronic (0, 0.625 mg/kg, sc for 10
             days) effects of lorcaserin on alcohol intake and preference
             were assessed at different time points. In a separate
             experiment, the effects of lorcaserin on locomotor activity
             were determined. Our results show that both 0.625 and 1.25
             mg/kg lorcaserin significantly reduced alcohol intake at 2,
             4 and 6 h. after the drug administration. The chronic
             administration of 0.625 mg/kg lorcaserin significantly
             reduced alcohol intake up to 6h every day after the
             injection and there was no sign of diminished efficacy of
             the drug during 10-day treatment. To determine the effects
             of lorcaserin on sucrose intake, rats were put on a
             two-bottle choice of water vs a solution of 7% sucrose. The
             high dose of lorcaserin (1.25 mg/kg, s.c.) reduced sucrose
             intake only for up to 2 h. When tested for locomotor
             activity, lorcaserin injected 20 min before testing
             significantly reduced locomotor activity at all doses.
             However, when it was injected 5.5h before the start of the
             1-h session, neither dose had a significant effect on
             locomotor activity. These results show the efficacy of
             lorcaserin in reducing alcohol intake without a significant
             effect on water intake and locomotion suggesting the
             involvement of 5-HT2c receptors in alcohol seeking behavior.
             Further research is warranted to determine the possible
             efficacy of lorcaserin or similar drugs as treatments for
             the treatment of alcoholism.},
   Doi = {10.1016/j.pbb.2014.07.017},
   Key = {fds275591}
}

@article{fds275592,
   Author = {Levin, ED and Hao, I and Burke, DA and Cauley, M and Hall, BJ and Rezvani,
             AH},
   Title = {Effects of tobacco smoke constituents, anabasine and
             anatabine, on memory and attention in female
             rats},
   Journal = {Journal of Psychopharmacology (Oxford, England)},
   Volume = {28},
   Number = {10},
   Pages = {915-922},
   Year = {2014},
   ISSN = {0269-8811},
   url = {http://dx.doi.org/10.1177/0269881114543721},
   Abstract = {© The Author(s) 2014.Nicotine has been well characterized
             to improve memory and attention. Nicotine is the primary,
             but not only neuroactive compound in tobacco. O tobacco
             constituents such as anabasine and anatabine also have
             agonist actions on nicotinic receptors. The current study
             investigated the effect anabasine and anatabine on memory
             and attention. Adult female Sprague-Dawley rats were trained
             on a win-shift spatial working and reference me task in the
             16-arm radial maze or a visual signal detection operant task
             to test attention. Acute dose-effect functions of anabasine
             and anata over two orders of magnitude were evaluated for
             both tasks. In the radial-arm maze memory test, anabasine
             but not anatabine significantly red the memory impairment
             caused by the NMDA antagonist dizocilpine (MK-801). In the
             signal detection attentional task, anatabine but not anaba
             significantly attenuated the attentional impairment caused
             by dizocilpine. These studies show that non-nicotine
             nicotinic agonists in tobacco, sim to nicotine, can
             significantly improve memory and attentional function. Both
             anabasine and anatabine produced cognitive improvement, but
             t effectiveness differed with regard to memory and
             attention. Follow-up studies with anabasine and anatabine
             are called for to determine their effi as therapeutics for
             memory and attentional dysfunction.},
   Doi = {10.1177/0269881114543721},
   Key = {fds275592}
}

@article{fds275597,
   Author = {Yenugonda, VM and Xiao, Y and Levin, ED and Rezvani, AH and Tran, T and Al-Muhtasib, N and Sahibzada, N and Xie, T and Wells, C and Slade, S and Johnson, JE and Dakshanamurthy, S and Kong, H-S and Tomita, Y and Liu,
             Y and Paige, M and Kellar, KJ and Brown, ML},
   Title = {Design, synthesis and discovery of picomolar selective
             α4β2 nicotinic acetylcholine receptor ligands.},
   Journal = {Journal of Medicinal Chemistry},
   Volume = {56},
   Number = {21},
   Pages = {8404-8421},
   Year = {2013},
   Month = {November},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/24047231},
   Abstract = {Developing novel and selective compounds that desensitize
             α4β2 nicotinic acetylcholine receptors (nAChRs) could
             provide new effective treatments for nicotine addiction, as
             well as other disorders. Here we report a new class of nAChR
             ligands that display high selectivity and picomolar binding
             affinity for α4β2 nicotinic receptors. The novel compounds
             have Ki values in the range of 0.031-0.26 nM and properties
             that should make them good candidates as drugs acting in the
             CNS. The selected lead compound 1 (VMY-2-95) binds with high
             affinity and potently desensitizes α4β2 nAChRs. At a dose
             of 3 mg/kg, compound 1 significantly reduced rat nicotine
             self-administration. The overall results support further
             characterizations of compound 1 and its analogues in
             preclinical models of nicotine addiction and perhaps other
             disorders involving nAChRs.},
   Doi = {10.1021/jm4008455},
   Key = {fds275597}
}

@article{fds275598,
   Author = {Levin, ED and Sexton, HG and Gordon, K and Gordon, CJ and Xiao, Y and Kellar, KJ and Yenugonda, VM and Liu, Y and White, MP and Paige, M and Brown, ML and Rezvani, AH},
   Title = {Effects of the sazetidine-a family of compounds on the body
             temperature in wildtype, nicotinic receptor β2-/- and
             α7-/- mice.},
   Journal = {European Journal of Pharmacology},
   Volume = {718},
   Number = {1-3},
   Pages = {167-172},
   Year = {2013},
   Month = {October},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/24036108},
   Abstract = {Nicotine elicits hypothermic responses in rodents. This
             effect appears to be related to nicotinic receptor
             desensitization because sazetidine-A, an α4β2 nicotinic
             receptor desensitizing agent, produces marked hypothermia
             and potentiates nicotine-induced hypothermia in mice. To
             determine the specificity of sazetidine-A induced
             hypothermia to β2 subunit-containing nicotinic receptors,
             we tested its efficacy in β2 knockout (β2(-/-)) mice.
             These effects were compared with wildtype (WT) and α7
             knockout (α7(-/-)) mice. Confirming our earlier results,
             sazetidine-A elicited a pronounced and long-lasting
             hypothermia in WT mice. In comparison, sazetidine-A induced
             a much attenuated and shorter hypothermic response in
             β2(-/-) mice. This indicates that the greater proportion of
             sazetidine-A induced hypothermia is mediated via actions on
             β2-containing nicotinic receptors, while a smaller
             component of hypothermia induced by sazetidine-A is mediated
             by non-β2 receptors. Similar to WT mice, α7(-/-) mice
             showed the full extent of the sazetidine-A effect,
             suggesting that the hypothermia produced by sazetidine-A did
             not depend on actions on α7 nicotinic receptor subtype.
             Three other novel nicotinic receptor desensitizing agents
             derived from sazetidine-A, triazetidine-O, VMY-2-95 and
             YL-1-127 also produced hypothermia in WT and α7(-/-) mice.
             Furthermore, unlike sazetidine-A, triazetidine-O and
             YL-1-127 did not show any hint of a hypothermic effect in
             β2(-/-) mice. VMY-2-95 like sazetidine-A did show a
             residual hypothermic effect in the β2(-/-) mice. These
             studies show that the hypothermic effects of sazetidine-A
             and the related compound VMY-2-95 are mainly mediated by
             nicotinic receptors containing β2 subunit, but that a small
             component of the effect is apparently mediated by non-β2
             containing receptors.},
   Doi = {10.1016/j.ejphar.2013.08.037},
   Key = {fds275598}
}

@article{fds275594,
   Author = {Levin, ED and Sexton, HG and Gordon, K and Gordon, CJ and Xiao, Y and Kellar, KJ and Yenugonda, VM and Liu, Y and White, MP and Paige, M and Brown, ML and Rezvani, AH},
   Title = {Effects of the sazetidine-a family of compounds on the body
             temperature in wildtype, nicotinic receptor
             β2-/- and α7-/- mice},
   Journal = {European Journal of Pharmacology},
   Volume = {718},
   Number = {1-3},
   Pages = {167-172},
   Year = {2013},
   Month = {September},
   ISSN = {0014-2999},
   url = {http://dx.doi.org/10.1016/j.ejphar.2013.08.037},
   Abstract = {Nicotine elicits hypothermic responses in rodents. This
             effect appears to be related to nicotinic receptor
             desensitization because sazetidine-A, an α4β2 nicotinic
             receptor desensitizing agent, produces marked hypothermia
             and potentiates nicotine-induced hypothermia in mice. To
             determine the specificity of sazetidine-A induced
             hypothermia to β2 subunit-containing nicotinic receptors,
             we tested its efficacy in β2 knockout (β2-/-) mice. These
             effects were compared with wildtype (WT) and α7 knockout
             (α7-/-) mice. Confirming our earlier results, sazetidine-A
             elicited a pronounced and long-lasting hypothermia in WT
             mice. In comparison, sazetidine-A induced a much attenuated
             and shorter hypothermic response in β2-/- mice. This
             indicates that the greater proportion of sazetidine-A
             induced hypothermia is mediated via actions on
             β2-containing nicotinic receptors, while a smaller
             component of hypothermia induced by sazetidine-A is mediated
             by non-β2 receptors. Similar to WT mice, α7-/- mice showed
             the full extent of the sazetidine-A effect, suggesting that
             the hypothermia produced by sazetidine-A did not depend on
             actions on α7 nicotinic receptor subtype. Three other novel
             nicotinic receptor desensitizing agents derived from
             sazetidine-A, triazetidine-O, VMY-2-95 and YL-1-127 also
             produced hypothermia in WT and α7-/- mice. Furthermore,
             unlike sazetidine-A, triazetidine-O and YL-1-127 did not
             show any hint of a hypothermic effect in β2 -/- mice.
             VMY-2-95 like sazetidine-A did show a residual hypothermic
             effect in the β2-/- mice. These studies show that the
             hypothermic effects of sazetidine-A and the related compound
             VMY-2-95 are mainly mediated by nicotinic receptors
             containing β2 subunit, but that a small component of the
             effect is apparently mediated by non-β2 containing
             receptors. © 2013 Elsevier B.V.},
   Doi = {10.1016/j.ejphar.2013.08.037},
   Key = {fds275594}
}

@article{fds275601,
   Author = {Liu, Y and Richardson, J and Tran, T and Al-Muhtasib, N and Xie, T and Yenugonda, VM and Sexton, HG and Rezvani, AH and Levin, ED and Sahibzada, N and Kellar, KJ and Brown, ML and Xiao, Y and Paige,
             M},
   Title = {Chemistry and pharmacological studies of
             3-alkoxy-2,5-disubstituted-pyridinyl compounds as novel
             selective α4β2 nicotinic acetylcholine receptor ligands
             that reduce alcohol intake in rats.},
   Journal = {Journal of Medicinal Chemistry},
   Volume = {56},
   Number = {7},
   Pages = {3000-3011},
   Year = {2013},
   Month = {April},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23540678},
   Abstract = {Neuronal acetylcholine receptors mediate the addictive
             effects of nicotine and may also be involved in alcohol
             addiction. Varenicline, an approved smoking cessation
             medication, showed clear efficacy in reducing alcohol
             consumption in heavy-drinking smokers. More recently,
             sazetidine-A, which selectively desensitizes α4β2
             nicotinic receptors, was shown to significantly reduce
             alcohol intake in a rat model. To develop novel therapeutics
             for treating alcohol use disorder, we designed and
             synthesized novel sazetidine-A analogues containing a methyl
             group at the 2-position of the pyridine ring. In vitro
             pharmacological studies revealed that some of the novel
             compounds showed overall pharmacological property profiles
             similar to that of sazetidine-A but exhibited reduced
             agonist activity across all nicotinic receptor subtypes
             tested. In rat studies, compound (S)-9 significantly reduced
             alcohol uptake. More importantly, preliminary results from
             studies in a ferret model indicate that these novel nAChR
             ligands have an improved adverse side-effect profile in
             comparison with that of varenicline.},
   Doi = {10.1021/jm4000374},
   Key = {fds275601}
}

@article{fds275602,
   Author = {Levin, ED and Cauley, M and Rezvani, AH},
   Title = {Improvement of attentional function with antagonism of
             nicotinic receptors in female rats.},
   Journal = {European Journal of Pharmacology},
   Volume = {702},
   Number = {1-3},
   Pages = {269-274},
   Year = {2013},
   Month = {February},
   ISSN = {1879-0712},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23399762},
   Abstract = {Nicotinic agonists have been shown in a variety of studies
             to improve cognitive function. Since nicotinic receptors are
             easily desensitized by agonists, it is not completely clear
             to what degree receptor desensitization or receptor
             activation are responsible for nicotinic agonist-induced
             cognitive improvement. In the current study, the effect of
             the neuronal nicotinic cholinergic α4β2 receptor
             antagonist dihydro-β-erythroidine (DHβE) and the α7
             nicotinic receptor antagonist methyllycaconitine (MLA) on
             attentional function was determined. Adult female
             Sprague-Dawley rats were trained on the visual signal
             detection task. They were required to discriminate whether
             or not a light signal occurred on a trial and respond with a
             lever press on one side after a signal and the opposite side
             after the absence of a signal in order to receive a food
             pellet reinforcer. Acute administration of the α4β2
             antagonist DHβE improved attentional function either alone
             or in reversing the attentional impairment caused by the
             NMDA glutamate antagonist dizocilpine (MK-801). Acute
             administration of MLA also significantly attenuated the
             dizocilpine-induced attentional impairment. In previous
             research we have shown that the α4β2 nicotinic
             desensitizing agent and partial agonist sazetidine-A also
             was effective in reversing dizocilpine-induced attentional
             impairments on the signal detection task and that low doses
             of the general nicotinic antagonist mecamylamine improved
             learning and memory. The current studies indicate that
             blockade of nicotinic receptors can effectively attenuate
             attentional impairments. Development of drugs that provide a
             net decrease in nicotinic receptor activity either through
             antagonism or desensitization could be worth exploring for
             beneficial effects for treating cognitive
             impairments.},
   Language = {eng},
   Doi = {10.1016/j.ejphar.2013.01.056},
   Key = {fds275602}
}

@article{fds275595,
   Author = {Overstreet, DH and Brown, R and Lawrence, AJ and Rezvani,
             AH},
   Title = {Overview of Animal Models of Drug Addiction},
   Pages = {149-157},
   Publisher = {Elsevier},
   Year = {2013},
   url = {http://dx.doi.org/10.1016/b978-0-12-398335-0.00016-9},
   Doi = {10.1016/b978-0-12-398335-0.00016-9},
   Key = {fds275595}
}

@article{fds275596,
   Author = {Rezvani, AH and Sexton, HG and Johnson, J and Wells, C and Gordon, K and Levin, ED},
   Title = {Effects of caffeine on alcohol consumption and nicotine
             self-administration in rats},
   Journal = {Alcoholism, Clinical and Experimental Research},
   Volume = {37},
   Number = {9},
   Pages = {1609-1617},
   Year = {2013},
   ISSN = {0145-6008},
   url = {http://dx.doi.org/10.1111/acer.12127},
   Abstract = {Background: Caffeine, alcohol, and nicotine are 3 of the
             most widespread self-administered psychoactive substances,
             which are known to be extensively co-administered. However,
             little is known about the degree to which they may mutually
             potentiate each other's consumption. Methods: In the current
             set of studies, we examined in rats the effect of caffeine
             administration on alcohol drinking and intravenous (i.v.)
             self-administration of nicotine. In male alcohol-preferring
             (P) rats, caffeine (5, 10, and 20 mg/kg) or the saline
             vehicle was administered acutely either by subcutaneous
             (S.C.) injection or orally (PO) by gavage. In a chronic
             study, the effect of PO caffeine (5 and 20 mg/kg) on alcohol
             intake over a 10-day period was tested. In another
             experiment, the effect of acute PO administration of
             caffeine (20 mg/kg) or saline on saccharin intake (0.2%
             solution) was determined in P rats. Effects of 20 mg/kg
             caffeine on motor activity were also determined in P rats.
             Finally, the effects of acute PO caffeine administration on
             nicotine self-administration in Sprague-Dawley rats were
             also determined. Results: Both routes of administration of
             caffeine, S.C. and PO, caused a significant dose-related
             decrease in alcohol intake and preference during free access
             to alcohol and after 4-day deprivation of alcohol. However,
             the low dose of 5 mg/kg caffeine increased alcohol intake.
             Acute PO caffeine also reduced saccharin intake. Acute
             systemic administration of 20 mg/kg caffeine did not exert a
             significant effect on motor activity. In Sprague-Dawley rats
             trained to self-administer i.v. nicotine, acute PO
             administration of caffeine significantly increased
             self-administration of nicotine in a dose-related manner.
             Conclusions: These results suggest that adenosine receptor
             systems may play a role in both alcohol and nicotine intake
             and deserve further study regarding these addictions. ©
             2013 by the Research Society on Alcoholism.},
   Doi = {10.1111/acer.12127},
   Key = {fds275596}
}

@article{fds275600,
   Author = {Rezvani, AH and Sexton, HG and Johnson, J and Wells, C and Gordon, K and Levin, ED},
   Title = {Effects of caffeine on alcohol consumption and nicotine
             self-administration in rats},
   Journal = {Alcoholism, Clinical and Experimental Research},
   Year = {2013},
   ISSN = {0145-6008},
   url = {http://dx.doi.org/10.1111/acer.12127},
   Abstract = {Background: Caffeine, alcohol, and nicotine are 3 of the
             most widespread self-administered psychoactive substances,
             which are known to be extensively co-administered. However,
             little is known about the degree to which they may mutually
             potentiate each other's consumption. Methods: In the current
             set of studies, we examined in rats the effect of caffeine
             administration on alcohol drinking and intravenous (i.v.)
             self-administration of nicotine. In male alcohol-preferring
             (P) rats, caffeine (5, 10, and 20 mg/kg) or the saline
             vehicle was administered acutely either by subcutaneous
             (S.C.) injection or orally (PO) by gavage. In a chronic
             study, the effect of PO caffeine (5 and 20 mg/kg) on alcohol
             intake over a 10-day period was tested. In another
             experiment, the effect of acute PO administration of
             caffeine (20 mg/kg) or saline on saccharin intake (0.2%
             solution) was determined in P rats. Effects of 20 mg/kg
             caffeine on motor activity were also determined in P rats.
             Finally, the effects of acute PO caffeine administration on
             nicotine self-administration in Sprague-Dawley rats were
             also determined. Results: Both routes of administration of
             caffeine, S.C. and PO, caused a significant dose-related
             decrease in alcohol intake and preference during free access
             to alcohol and after 4-day deprivation of alcohol. However,
             the low dose of 5 mg/kg caffeine increased alcohol intake.
             Acute PO caffeine also reduced saccharin intake. Acute
             systemic administration of 20 mg/kg caffeine did not exert a
             significant effect on motor activity. In Sprague-Dawley rats
             trained to self-administer i.v. nicotine, acute PO
             administration of caffeine significantly increased
             self-administration of nicotine in a dose-related manner.
             Conclusions: These results suggest that adenosine receptor
             systems may play a role in both alcohol and nicotine intake
             and deserve further study regarding these addictions. ©
             2013 by the Research Society on Alcoholism.},
   Doi = {10.1111/acer.12127},
   Key = {fds275600}
}

@article{fds275715,
   Author = {Rezvani, AH and Cauley, M and Xiao, Y and Kellar, KJ and Levin,
             ED},
   Title = {Effects of chronic sazetidine-A, a selective α4β2 neuronal
             nicotinic acetylcholine receptors desensitizing agent on
             pharmacologically- induced impaired attention in
             rats},
   Journal = {Psychopharmacology},
   Volume = {226},
   Number = {1},
   Pages = {35-43},
   Year = {2013},
   ISSN = {0033-3158},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23100170},
   Abstract = {Rationale: Nicotine and nicotinic agonists have been shown
             to improve attentional function. Nicotinic receptors are
             easily desensitized, and all nicotinic agonists are also
             desensitizing agents. Although both receptor activation and
             desensitization are components of the mechanism that
             mediates the overall effects of nicotinic agonists, it is
             not clear how each of the two opposed actions contributes to
             attentional improvements. Sazetidine-A has high binding
             affinity at α4β2 nicotinic receptors and causes a
             relatively brief activation followed by a long-lasting
             desensitization of the receptors. Acute administration of
             sazetidine-A has been shown to significantly improve
             attention by reversing impairments caused by the muscarinic
             cholinergic antagonist scopolamine and the NMDA glutamate
             antagonist dizocilpine. Methods: In the current study, we
             tested the effects of chronic subcutaneous infusion of
             sazetidine-A (0, 2, or 6 mg/kg/day) on attention in
             Sprague-Dawley rats. Furthermore, we investigated the
             effects of chronic sazetidine-A treatment on attentional
             impairment induced by an acute administration of 0.02 mg/kg
             scopolamine. Results: During the first week period, the
             6-mg/kg/day sazetidine-A dose significantly reversed the
             attentional impairment induced by scopolamine. During weeks
             3 and 4, the scopolamine-induced impairment was no longer
             seen, but sazetidine-A (6 mg/kg/day) significantly improved
             attentional performance on its own. Chronic sazetidine-A
             also reduced response latency and response omissions.
             Conclusions: This study demonstrated that similar to its
             acute effects, chronic infusions of sazetidine-A improve
             attentional performance. The results indicate that the
             desensitization of α4β2 nicotinic receptors with some
             activation of these receptors may play an important role in
             improving effects of sazetidine-A on attention. © 2012
             Springer-Verlag Berlin Heidelberg.},
   Language = {eng},
   Doi = {10.1007/s00213-012-2895-6},
   Key = {fds275715}
}

@article{fds275720,
   Author = {Hussmann, GP and Turner, JR and Lomazzo, E and Venkatesh, R and Cousins,
             V and Xiao, Y and Yasuda, RP and Wolfe, BB and Perry, DC and Rezvani, AH and Levin, ED and Blendy, JA and Kellar, KJ},
   Title = {Chronic sazetidine-A at behaviorally active doses does not
             increase nicotinic cholinergic receptors in rodent
             brain.},
   Journal = {Journal of Pharmacology and Experimental
             Therapeutics},
   Volume = {343},
   Number = {2},
   Pages = {441-450},
   Year = {2012},
   Month = {November},
   ISSN = {1521-0103},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22899752},
   Keywords = {Animals • Azetidines • Behavior, Animal •
             Benzazepines • Binding Sites • Brain Chemistry
             • Cerebral Cortex • Dose-Response Relationship,
             Drug • Female • Male • Membranes •
             Neurons • Nicotine • Nicotinic Agonists •
             Pregnancy • Pyridines • Quinoxalines • Rats
             • Rats, Sprague-Dawley • Receptors, Nicotinic
             • Self Administration • Up-Regulation •
             administration & dosage • blood • cytology •
             drug effects • drug effects* • metabolism •
             pharmacology • pharmacology*},
   Abstract = {Chronic nicotine administration increases α4β2 neuronal
             nicotinic acetylcholine receptor (nAChR) density in brain.
             This up-regulation probably contributes to the development
             and/or maintenance of nicotine dependence. nAChR
             up-regulation is believed to be triggered at the ligand
             binding site, so it is not surprising that other nicotinic
             ligands also up-regulate nAChRs in the brain. These other
             ligands include varenicline, which is currently used for
             smoking cessation therapy. Sazetidine-A (saz-A) is a newer
             nicotinic ligand that binds with high affinity and
             selectivity at α4β2* nAChRs. In behavioral studies, saz-A
             decreases nicotine self-administration and increases
             performance on tasks of attention. We report here that,
             unlike nicotine and varenicline, chronic administration of
             saz-A at behaviorally active and even higher doses does not
             up-regulate nAChRs in rodent brains. We used a newly
             developed method involving radioligand binding to measure
             the concentrations and nAChR occupancy of saz-A, nicotine,
             and varenicline in brains from chronically treated rats. Our
             results indicate that saz-A reached concentrations in the
             brain that were ∼150 times its affinity for α4β2* nAChRs
             and occupied at least 75% of nAChRs. Thus, chronic
             administration of saz-A did not up-regulate nAChRs despite
             it reaching brain concentrations that are known to bind and
             desensitize virtually all α4β2* nAChRs in brain. These
             findings reinforce a model of nicotine addiction based on
             desensitization of up-regulated nAChRs and introduce a
             potential new strategy for smoking cessation therapy in
             which drugs such as saz-A can promote smoking cessation
             without maintaining nAChR up-regulation, thereby potentially
             increasing the rate of long-term abstinence from
             nicotine.},
   Language = {eng},
   Doi = {10.1124/jpet.112.198085},
   Key = {fds275720}
}

@article{fds275722,
   Author = {Swartzwelder, NA and Risher, ML and Abdelwahab, SH and D'Abo, A and Rezvani, AH and Levin, ED and Wilson, WA and Swartzwelder, HS and Acheson, SK},
   Title = {Effects of ethanol, Δ(9)-tetrahydrocannabinol, or their
             combination on object recognition memory and object
             preference in adolescent and adult male rats.},
   Journal = {Neuroscience Letters},
   Volume = {527},
   Number = {1},
   Pages = {11-15},
   Year = {2012},
   Month = {October},
   ISSN = {1872-7972},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22959891},
   Abstract = {Recent advances have been made in our understanding of the
             deleterious effects of both ethanol and THC on adolescent
             behavior and brain development. However, very little is
             known about the combined effects of EtOH+THC during
             adolescence, a time in which these drugs are often used
             together. The purpose of this experiment was to: (1)
             determine whether EtOH and/or THC induced greater working
             memory impairment in adolescent than adult male rats using
             the novel object recognition (NOR) task and (2) determine
             whether the EtOH+THC combination would produce a more potent
             additive effect in adolescents than adults when compared to
             these drugs alone. NOR was performed with a 24h delay under
             each of the four drug conditions: vehicle; 1.5g/kg ethanol;
             1.0mg/kg THC; and 1.5g/kg EtOH+1.0mg/kg THC, at 72h
             intervals. The results show that there was an age effect on
             working memory in NOR after the EtOH+THC challenge.
             Specifically, adolescent animals showed a preference for the
             familiar object whereas adults showed no preference for the
             novel or familiar object, the latter being characteristic of
             a classic working memory deficit. These effects were not
             dependent on changes in exploration across session, global
             activity across drug condition, or total object exploration.
             These novel findings clearly indicate that further
             understanding of this age-drug interaction is crucial to
             elucidating the influence that adolescent EtOH+THC use may
             have on repeated drug use and abuse later in
             life.},
   Language = {eng},
   Doi = {10.1016/j.neulet.2012.08.037},
   Key = {fds275722}
}

@article{fds275719,
   Author = {Rezvani, AH and Cauley, MC and Johnson, EC and Gatto, GJ and Levin,
             ED},
   Title = {Effects of AZD3480, a neuronal nicotinic acetylcholine
             receptor agonist, and donepezil on dizocilpine-induced
             attentional impairment in rats.},
   Journal = {Psychopharmacology},
   Volume = {223},
   Number = {3},
   Pages = {251-258},
   Year = {2012},
   Month = {October},
   ISSN = {1432-2072},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22526540},
   Keywords = {Animals • Attention Deficit Disorder with Hyperactivity
             • Behavior, Animal • Disease Models, Animal •
             Dizocilpine Maleate • Dose-Response Relationship, Drug
             • Female • Indans • Molecular Structure
             • Neurons • Nicotinic Agonists • Piperidines
             • Pyridines • Rats • Rats, Sprague-Dawley
             • Receptors, N-Methyl-D-Aspartate • Receptors,
             Nicotinic • Signal Detection, Psychological •
             antagonists & inhibitors • chemically induced •
             chemistry • drug effects • drug effects* •
             metabolism • pharmacology • prevention & control*
             • psychology • therapeutic use*},
   Abstract = {Nicotinic acetylcholine systems play major roles in
             cognitive function. Nicotine and a variety of nicotinic
             agonists improve attention, and nicotinic antagonist
             exposure impairs it. This study was conducted to investigate
             the effect of a novel nicotinic receptor agonist at α4β2
             nicotinic receptors (AZD3480) on attention and reversal of
             pharmacologically induced attentional impairment produced by
             the NMDA glutamate antagonist dizocilpine (MK-801).Adult
             female Sprague-Dawley rats were trained to perform an
             operant visual signal detection task to a stable baseline of
             accuracy. The rats were then injected subcutaneously
             following a repeated measures, counter-balanced design with
             saline, AZD3480 (0.01, 0.1, and 1 mg/kg), dizocilpine (0.05
             mg/kg), or their combinations 30 min before the test. The
             effect of donepezil on the same pharmacologically induced
             attentional impairment was also tested. A separate group of
             rats was injected with donepezil (0.01, 0.1, and 1 mg/kg),
             dizocilpine (0.05 mg/kg), or their combinations, and their
             attention were assessed. Saline was the vehicle
             control.Dizocilpine caused a significant (p < 0.0005)
             impairment in percent correct performance. This attentional
             impairment was significantly (p < 0.0005) reversed by
             0.01 and 0.1 mg/kg of AZD3480. AZD3480 by itself did not
             alter the already high baseline control performance.
             Donepezil (0.01-1.0 mg/kg) also significantly
             (p < 0.005) attenuated the dizocilpine-induced
             attentional impairment.AZD3480, similar to donepezil, showed
             significant efficacy for counteracting the attentional
             impairment caused by the NMDA glutamate antagonist
             dizocilpine. Low doses of AZD3480 may provide therapeutic
             benefit for reversing attentional impairment in patients
             suffering from cognitive impairment due to glutamatergic
             dysregulation and likely other attentional
             disorders.},
   Language = {eng},
   Doi = {10.1007/s00213-012-2712-2},
   Key = {fds275719}
}

@article{fds275718,
   Author = {Rezvani, AH and Lawrence, AJ and Arolfo, MP and Levin, ED and Overstreet, DH},
   Title = {Novel medication targets for the treatment of alcoholism:
             preclinical studies.},
   Journal = {Recent Patents on CNS Drug Discovery},
   Volume = {7},
   Number = {2},
   Pages = {151-162},
   Year = {2012},
   Month = {August},
   ISSN = {2212-3954},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22574676},
   Keywords = {Alcohol Deterrents • Alcoholism • Animals •
             Azepines • Azetidines • Carbamates • Disease
             Models, Animal • Drug Evaluation, Preclinical •
             Drugs, Investigational • Humans • Isoflavones
             • Molecular Targeted Therapy • Patents as Topic
             • Piperidines • Pyridines • Synaptic
             Transmission • drug effects • drug therapy* •
             methods • methods* • pharmacology •
             pharmacology* • psychology* • therapeutic
             use},
   Abstract = {Alcoholism is a complex heterogeneous disease and a number
             of neurotransmitter and neuromodulator systems have been
             implicated in its manifestation. Consequently, it is
             unlikely that existing medications such as disulfiram
             (Antabuse®), naltrexone (ReVia®), acamprosate (Campral®))
             can be efficacious in every individual. Thus, the
             development of novel therapeutic agents with greater
             selectivity and less unwanted effects for the treatment of
             this disease is one of the major objectives of alcohol
             research. This review summarizes the findings of five novel
             compounds with different neuronal targets for treating
             alcoholism. These compounds include sazetidine-A, which
             selectively desensitizes α4β2 nicotinic receptors;
             carisbamate, a novel anti-epileptic agent; JNJ5234801, a
             novel anxiolytic agent; GS-455534, a highly selective
             inhibitor of mitochondrial aldehyde dehydrogenase; and
             JNJ-39220675, a selective histamine H3 antagonist. Inbred
             alcohol-preferring rats (iP), Fawn-Hooded (FH) rats, and P
             rats were used to evaluate the compounds. Naltrexone was
             used as a positive control in some experiments. All five
             compounds reduced alcohol consumption and preference. The
             mechanisms thought to underlie these effects suggest that,
             in addition to dopaminergic and opioidergic systems, other
             neuronal systems such as sodium channels (carisbamate),
             mitochondrial aldehyde dehydrogenase (GS-455534), 5-HT2
             receptors (JNJ-5234801), histamine H3 receptors
             (JNJ-39220675), and α4β2 nicotinic receptors
             (sazetidine-A) can be involved in alcohol drinking. Further
             work is necessary to confirm the exact mechanisms of action
             of each drug and to determine any viable targets for
             putative treatment of alcohol-use disorders. The article
             presents some promising patents on novel medication targets
             for the treatment of alcoholism.},
   Language = {eng},
   Key = {fds275718}
}

@article{fds275717,
   Author = {Johnson, JE and Slade, S and Wells, C and Petro, A and Sexton, H and Rezvani, AH and Brown, ML and Paige, MA and McDowell, BE and Xiao, Y and Kellar, KJ and Levin, ED},
   Title = {Assessing the effects of chronic sazetidine-A delivery on
             nicotine self-administration in both male and female
             rats.},
   Journal = {Psychopharmacology},
   Volume = {222},
   Number = {2},
   Pages = {269-276},
   Year = {2012},
   Month = {July},
   ISSN = {1432-2072},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22297831},
   Keywords = {Animals • Azetidines • Dose-Response Relationship,
             Drug • Female • Male • Nicotine •
             Nicotinic Agonists • Pyridines • Rats • Rats,
             Sprague-Dawley • Receptors, Nicotinic • Self
             Administration • Sex Factors • Smoking Cessation
             • administration & dosage • administration &
             dosage* • drug effects* • metabolism •
             methods • pharmacology*},
   Abstract = {RATIONALE: Sazetidine-A is a selective α4β2 nicotinic
             receptor desensitizing agent and partial agonist. It has
             been shown in previous studies to significantly reduce
             nicotine self-administration in rats after acute or repeated
             injections. However, the effects of continuous chronic
             infusions of sazetidine-A on maintenance of nicotine
             self-administration and relapse after abstinence have yet to
             be examined. OBJECTIVES: This study evaluated the efficacy
             of continuous sazetidine-A infusions (sc) over a period of 4
             weeks to reduce nicotine self-administration in male and
             female Sprague-Dawley rats. METHODS: Sazetidine-A was
             administered via Alzet osmotic minipumps to young adult
             female and male rats at doses of 0, 2 or 6 mg/kg/day for 4
             weeks. The effects of sazetidine-A on IV nicotine
             self-administration were examined in repeated 3-h sessions
             over the first 2 weeks of infusion followed by 1 week of
             forced abstinence from nicotine and 1 week of resumed
             nicotine access. RESULTS: The 6 mg/kg/day sazetidine-A dose
             significantly reduced overall nicotine self-administration
             compared with vehicle control across the sessions for both
             male (p < 0.001) and female (p < 0.05) rats. The
             lower 2 mg/kg/day sazetidine-A infusion dose was effective
             in reducing nicotine self-administration for male
             (p < 0.001), but not female rats. No attenuation in
             sazetidine-A effectiveness was seen over the course of the
             4-week treatment. In the vehicle control group, male rats
             self-administered significantly (p < 0.001) more
             nicotine than females. CONCLUSIONS: The continuing
             effectiveness of sazetidine-A in reducing nicotine
             self-administration in both male and female rats supports
             its promise as a new treatment to help people successfully
             quit smoking.},
   Language = {eng},
   Doi = {10.1007/s00213-012-2642-z},
   Key = {fds275717}
}

@article{fds275671,
   Author = {Bartley, PC and Rezvani, AH},
   Title = {Alcohol and cognition - consideration of age of initiation,
             usage patterns and gender: a brief review.},
   Journal = {Current Drug Abuse Reviews},
   Volume = {5},
   Number = {2},
   Pages = {87-97},
   Year = {2012},
   Month = {June},
   ISSN = {1874-4745},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22455507},
   Keywords = {Age Factors • Alcohol Drinking • Cognition •
             Humans • Sex Characteristics • drug effects*
             • psychology*},
   Abstract = {Heavy alcohol use has numerous negative impacts on
             cognition. In many cases, it appears that excess drinking
             influences working memory, problem solving, attention,
             patterns of regional brain activation, and even gray and
             white matter volume. Due to these effects, most significant
             conclusions related to cognitive decline are limited to the
             assumption that "more is worse." However, heavy alcohol use
             is a very complex psychosocial behavior and is subject to a
             problematic number of variables. As a result, it is very
             difficult to extend generalizations about drinking-related
             consequences to the overall population since many
             environmental and biological differences come into play for
             every individual. Three of these variables shown to have
             significant impact on cognitive sensitivity to alcohol are
             age of first alcohol use (age of drinking initiation),
             specific pattern of alcohol consumption and gender.
             Potential insight can be gained into how individual drinking
             scenarios differ in risk for cognitive decline by assessing
             how each of these important factors influences cognition
             independently. Although some overlap exists between
             categories, each still appears to contribute unique
             influence on likelihood and presentation of
             cognition-related effects. Based on existing and current
             research, age and gender tend to augment baseline
             sensitivity to alcohol, with patterns of alcohol intake also
             influencing how changes appear. Given these categorical
             differences, it is important to consider personal alcohol
             drinking history rather than just aggregate alcohol intake
             as risk factors in the cognitive impacts of drinking. The
             objective of this brief review is to examine the role of
             these factors on the effect of alcohol on
             cognition.},
   Language = {eng},
   Key = {fds275671}
}

@article{fds275716,
   Author = {Rezvani, AH and Timofeeva, O and Sexton, HG and DeCuir, D and Xiao, Y and Gordon, CJ and Kellar, KJ and Levin, ED},
   Title = {Effects of sazetidine-A, a selective α4β2* nicotinic
             receptor desensitizing agent, on body temperature regulation
             in mice and rats.},
   Journal = {European Journal of Pharmacology},
   Volume = {682},
   Number = {1-3},
   Pages = {110-117},
   Year = {2012},
   Month = {May},
   ISSN = {1879-0712},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22387853},
   Keywords = {Aconitine • Animals • Azetidines • Body
             Temperature Regulation • Dihydro-beta-Erythroidine
             • Dose-Response Relationship, Drug • Drug
             Interactions • Male • Mice • Nicotine •
             Nicotinic Antagonists • Pyridines • Rats •
             Receptors, Nicotinic • analogs & derivatives •
             drug effects* • metabolism* • pharmacology •
             pharmacology*},
   Abstract = {Nicotine-induced hypothermia is well established, but the
             nicotinic receptor actions underlying this effect are not
             clear. Nicotine causes activation and desensitization at a
             variety of nicotinic receptor subtypes. Sazetidine-A
             [6-(5(((S)-azetidine-2-yl)methoxy)pyridine-3-yl)hex-5-yn-1-ol]
             is a novel compound that potently and selectively
             desensitizes α4β2* nicotinic receptors. The main goal of
             this study was to investigate the effects of sazetidine-A,
             on core body temperature (Tc) in mice and rats. Sazetidine-A
             effects on Tc and the interactions of sazetidine-A with
             nicotine and selective nicotinic antagonists were
             investigated to determine the receptor actions underlying
             nicotine-induced hypothermia. Adult male mice were injected
             with different dose of nicotine (0.2, 0.4 and 0.8 mg/kg),
             sazetidine-A (0.3, 1, and 3mg/kg), a mixture of nicotine
             (0.4 or 0.8 mg/kg) and sazetidine-A (0.3 or 0.6 mg/kg) or
             saline and Tc was monitored telemetrically. In another set
             of experiments, the interaction between sazetidine-A and
             dihydro-β-erythroidine (DHβE), an α4β2* nicotinic
             receptors antagonist, and methyllycaconitine (MLA), an α7
             antagonist, was investigated. Tc of mice was monitored
             following DHβE (1, 3 and 6 mg/kg), a combination of DHβE
             (3mg/kg) and sazetidine-A (0.6 mg/kg), MLA (1.5, 3 or 6
             mg/kg) or combination of MLA (6 mg/kg) and sazetidine (0.6
             mg/kg) or saline. The acute effect of sazetidine-A (1, 3,
             and 6 mg/kg) on rats Tc was also studied. Acute sazetidine-A
             caused a pronounced and long-lasting hypothermia in mice; Tc
             decreased to about 28°C at 100 min and recovered within 230
             min. The hypothermic effect of sazetidine in rats was much
             less in magnitude (about 3°C) and shorter in duration
             compared with that in mice. Nicotine co-administration with
             low doses of sazetidine potentiated the magnitude and
             duration of hypothermia in mice. The α4β2* nicotinic
             receptors antagonist DHβE significantly prolonged
             sazetidine-A-induced hypothermia but did not increase its
             depth. The α7 antagonist MLA caused a modest degree of
             hypothermia with relatively short duration in mice. MLA
             failed to counteract the sazetidine-A-induced hypothermia.
             Overall, our results show that pharmacological modulation of
             α4β2* nicotinic receptors elicits changes in body
             temperature that may involve desensitization of these
             receptors.},
   Language = {eng},
   Doi = {10.1016/j.ejphar.2012.02.031},
   Key = {fds275716}
}

@article{fds275714,
   Author = {Levin, ED and Slade, S and Wells, C and Cauley, M and Petro, A and Vendittelli, A and Johnson, M and Williams, P and Horton, K and Rezvani,
             AH},
   Title = {Threshold of adulthood for the onset of nicotine
             self-administration in male and female rats.},
   Journal = {Behavioural Brain Research},
   Volume = {225},
   Number = {2},
   Pages = {473-481},
   Year = {2011},
   Month = {December},
   ISSN = {1872-7549},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21854810},
   Keywords = {Age Factors • Animals • Cocaine •
             Conditioning, Operant • Critical Period (Psychology)*
             • Estrus • Female • Male • Nicotine
             • Rats • Rats, Sprague-Dawley • Reinforcement
             Schedule • Self Administration • Sex
             Characteristics • administration & dosage • drug
             effects* • pharmacology • pharmacology*},
   Abstract = {The great majority of tobacco addiction begins during
             adolescence. More heavily addicted smokers begin smoking
             earlier, but differentiating the neurobehavioral impact of
             nicotine self-administration during adolescence from
             self-selection bias (whereby people more prone to heavy
             addiction also begin earlier) cannot be ethically
             unconfounded in humans. The goals of this research were to
             determine the age threshold for the adult-like nicotine
             self-administration and determine sex differences. Male and
             female Sprague-Dawley rats were tested for nicotine
             self-administration starting at 4, 5, 6, 7, and 8 weeks of
             age in an operant FR1 schedule for IV nicotine (0.03
             mg/kg/infusion) in 45-min sessions for 2 weeks, with 1 week
             of enforced abstinence and 1 week of resumed access. This
             study replicated our earlier work that nicotine
             self-administration was increased in adolescent vs. adult
             rats and that the effect was more pronounced in adolescent
             males, but the increased nicotine self-administration was
             more persistent in adolescent-onset females. The age
             threshold for adult-like behavior was 6-7 weeks of age.
             Adolescent-onset nicotine self-administration had persisting
             effects of eggaurated increases of nicotine
             self-administration when fixed-ratio requirements for
             self-administration were lowered. Female rats that had begun
             nicotine self-administration during adolescence showed
             exaggerated increases in nicotine self-administration after
             a switch back to FR1 from FR8, indicating a lessened control
             over their self-administration. Adolescent-onset nicotine
             self-administration was not found to potentiate cocaine
             self-administration. Adolescent-onset nicotine
             self-administration causes persistent increases in nicotine
             self-administration in female rats even after they reach
             adulthood and disrupts control over self-administration
             behavior.},
   Language = {eng},
   Doi = {10.1016/j.bbr.2011.08.005},
   Key = {fds275714}
}

@article{fds275713,
   Author = {Cippitelli, A and Rezvani, AH and Robinson, JE and Eisenberg, L and Levin, ED and Bonaventure, P and Motley, ST and Lovenberg, TW and Heilig, M and Thorsell, A},
   Title = {The novel, selective, brain-penetrant neuropeptide Y Y2
             receptor antagonist, JNJ-31020028, tested in animal models
             of alcohol consumption, relapse, and anxiety.},
   Journal = {Alcohol},
   Volume = {45},
   Number = {6},
   Pages = {567-576},
   Year = {2011},
   Month = {September},
   ISSN = {1873-6823},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21145691},
   Keywords = {Alcohol Drinking • Alcoholism • Animals •
             Anxiety Disorders • Benzamides • Conditioning,
             Operant • Ethanol • Injections, Intraventricular
             • Models, Animal • Neuropeptide Y •
             Piperazines • Rats • Rats, Wistar •
             Receptors, Neuropeptide Y • Recurrence •
             Reinforcement (Psychology) • Self Administration •
             Substance Withdrawal Syndrome • adverse effects •
             antagonists & inhibitors* • chemically induced •
             drug effects • drug therapy • drug therapy* •
             pharmacology • pharmacology*},
   Abstract = {Neuropeptide Y (NPY) signaling has been shown to modulate
             stress responses and to be involved in regulation of alcohol
             intake and dependence. The present study explores the
             possibility that blockade of NPY Y2 autoreceptors using a
             novel, blood-brain barrier penetrant NPY Y2 receptor
             antagonist, JNJ-31020028 (N-(4-{4-[2-(diethylamino)-2-oxo-1-phenylethyl]piperazin-1-yl}-3-fluorophenyl)-2-pyridin-3-ylbenzamide),
             may achieve a therapeutically useful activation of the NPY
             system in alcohol- and anxiety-related behavioral models. We
             examined JNJ-31020028 in operant alcohol
             self-administration, stress-induced reinstatement to alcohol
             seeking, and acute alcohol withdrawal (hangover)-induced
             anxiety. Furthermore, we tested its effects on voluntary
             alcohol consumption in a genetic animal model of alcohol
             preference, the alcohol-preferring (P) rat. Neither systemic
             (0, 15, 30, and 40 mg/kg, subcutaneously [s.c.]) nor
             intracerebroventricular (0.0, 0.3, and 1.0 nmol/rat)
             administration of JNJ-31020028 affected alcohol-reinforced
             lever pressing or relapse to alcohol seeking behavior
             following stress exposure. Also, when its effects were
             tested on unlimited access to alcohol in P rats, preference
             for alcohol solution was transiently suppressed but without
             affecting voluntary alcohol intake. JNJ-31020028 (15 mg/kg,
             s.c.) did reverse the anxiogenic effects of withdrawal from
             a single bolus dose of alcohol on the elevated plus-maze,
             confirming the anxiolytic-like properties of NPY Y2
             antagonism. Our data do not support Y2 antagonism as a
             mechanism for reducing alcohol consumption or relapse-like
             behavior, but the observed effects on withdrawal-induced
             anxiety suggest that NPY Y2 receptor antagonists may be a
             putative treatment for the negative affective states
             following alcohol withdrawal.},
   Language = {eng},
   Doi = {10.1016/j.alcohol.2010.09.003},
   Key = {fds275713}
}

@article{fds275712,
   Author = {Levin, ED and Bushnell, PJ and Rezvani, AH},
   Title = {Attention-modulating effects of cognitive
             enhancers.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {99},
   Number = {2},
   Pages = {146-154},
   Year = {2011},
   Month = {August},
   ISSN = {1873-5177},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21334367},
   Keywords = {Animals • Attention • Attention Deficit Disorder
             with Hyperactivity • Behavior, Animal • Disease
             Models, Animal • Dizocilpine Maleate • Humans
             • Mecamylamine • Nootropic Agents • Rats
             • Rats, Inbred SHR • Scopolamine Hydrobromide
             • drug effects • drug effects* • drug therapy
             • etiology • pharmacology • pharmacology*
             • physiology • physiopathology},
   Abstract = {Attention can be readily measured in experimental animal
             models. Animal models of attention have been used to better
             understand the neural systems involved in attention, how
             attention is impaired, and how therapeutic treatments can
             ameliorate attentional deficits. This review focuses on the
             ways in which animal models are used to better understand
             the neuronal mechanism of attention and how to develop new
             therapeutic treatments for attentional impairment. Several
             behavioral test methods have been developed for experimental
             animal studies of attention, including a 5-choice serial
             reaction time task (5-CSRTT), a signal detection task (SDT),
             and a novel object recognition (NOR) test. These tasks can
             be used together with genetic, lesion, pharmacological and
             behavioral models of attentional impairment to test the
             efficacy of novel therapeutic treatments. The most prominent
             genetic model is the spontaneously hypertensive rat (SHR).
             Well-characterized lesion models include frontal cortical or
             hippocampal lesions. Pharmacological models include
             challenge with the NMDA glutamate antagonist dizocilpine
             (MK-801), the nicotinic cholinergic antagonist mecamylamine
             and the muscarinic cholinergic antagonist scopolamine.
             Behavioral models include distracting stimuli and attenuated
             target stimuli. Important validation of these behavioral
             tests and models of attentional impairments for developing
             effective treatments for attentional dysfunction is the fact
             that stimulant treatments effective for attention deficit
             hyperactivity disorder (ADHD), such as methylphenidate
             (Ritalin®), are effective in the experimental animal
             models. Newer lines of treatment including nicotinic
             agonists, α4β2 nicotinic receptor desensitizers, and
             histamine H₃ antagonists, have also been found to be
             effective in improving attention in these animal models.
             Good carryover has also been seen for the attentional
             improvement caused by nicotine in experimental animal models
             and in human populations. Animal models of attention can be
             effectively used for the development of new treatments of
             attentional impairment in ADHD and other syndromes in which
             have attentional impairments occur, such as Alzheimer's
             disease and schizophrenia.},
   Language = {eng},
   Doi = {10.1016/j.pbb.2011.02.008},
   Key = {fds275712}
}

@article{fds275711,
   Author = {Rezvani, AH and Cauley, M and Sexton, H and Xiao, Y and Brown, ML and Paige, MA and McDowell, BE and Kellar, KJ and Levin,
             ED},
   Title = {Sazetidine-A, a selective α4β2 nicotinic acetylcholine
             receptor ligand: effects on dizocilpine and
             scopolamine-induced attentional impairments in female
             Sprague-Dawley rats.},
   Journal = {Psychopharmacology},
   Volume = {215},
   Number = {4},
   Pages = {621-630},
   Year = {2011},
   Month = {June},
   ISSN = {1432-2072},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21274704},
   Keywords = {Animals • Attention • Azetidines • Behavior,
             Animal • Cognition • Dizocilpine Maleate •
             Dose-Response Relationship, Drug • Drug Interactions
             • Female • Ligands • Molecular Structure
             • Photic Stimulation • Psychomotor Performance
             • Pyridines • Rats • Rats, Sprague-Dawley
             • Receptors, Nicotinic • Scopolamine Hydrobromide
             • chemistry • drug effects • drug effects*
             • metabolism* • pharmacology*},
   Abstract = {Neuronal nicotinic receptor systems have been shown to play
             key roles in cognition. Nicotine and nicotinic analogs
             improve attention and nicotinic antagonists impair it. This
             study was conducted to investigate the role of α4β2
             nicotinic receptors in sustained attention using a novel
             selective α4β2 nicotinic receptor ligand,
             sazetidine-A.Female rats were trained to perform the signal
             detection task to a stable baseline of accuracy. The rats
             were injected with saline, sazetidine-A (0.01, 0.03, and
             0.1 mg/kg), dizocilpine (0.05 mg/kg), or their
             combination; or, in another experiment, the rats were
             injected with the same doses of sazetidine-A, scopolamine
             (0.02 mg/kg), or their combination.Percent hit and percent
             correct rejection showed that dizocilpine caused significant
             (p < 0.025) impairments in performance, which were
             significantly reversed by each of the sazetidine-A doses.
             Response omissions were significantly (p < 0.05)
             increased by dizocilpine, and this was also significantly
             reversed by each of the sazetidine-A doses. None of the
             sazetidine-A doses had significant effects on hit, correct
             rejection, or response omissions when given alone.
             Scopolamine also caused significant (p < 0.0005)
             impairments in percent hit and percent correct rejection and
             increased response omissions, which were significantly
             attenuated by all the sazetidine-A doses for percent hit and
             response omissions and by the highest dose of sazetidine-A
             for percent correct rejection. Both scopolamine and
             dizocilpine significantly (p < 0.0005) increased
             response latency, an effect which was significantly
             attenuated by sazetidine-A coadministration.These studies
             imply an important role for α4β2 nicotinic receptors in
             improving sustained attention under conditions that disrupt
             it. Very low doses of sazetidine-A or drugs with a similar
             profile may provide therapeutic benefit for reversing
             attentional impairment in patients suffering from mental
             disorders and/or cognitive impairment.},
   Language = {eng},
   Doi = {10.1007/s00213-010-2161-8},
   Key = {fds275711}
}

@article{fds275710,
   Author = {Galici, R and Rezvani, AH and Aluisio, L and Lord, B and Levin, ED and Fraser, I and Boggs, J and Welty, N and Shoblock, JR and Motley, ST and Letavic, MA and Carruthers, NI and Dugovic, C and Lovenberg, TW and Bonaventure, P},
   Title = {JNJ-39220675, a novel selective histamine H3 receptor
             antagonist, reduces the abuse-related effects of alcohol in
             rats.},
   Journal = {Psychopharmacology},
   Volume = {214},
   Number = {4},
   Pages = {829-841},
   Year = {2011},
   Month = {April},
   ISSN = {1432-2072},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21086115},
   Keywords = {Alcoholism • Animals • Autoradiography •
             Azepines • Behavior, Animal • Brain •
             Histamine H3 Antagonists • Injections, Subcutaneous
             • Male • Microdialysis • Molecular Structure
             • Motor Activity • Protein Binding •
             Pyridines • Rats • Rats, Sprague-Dawley •
             Receptors, Histamine H3 • Reinforcement (Psychology)
             • Self Administration • drug effects • drug
             therapy* • metabolism • pharmacokinetics •
             pharmacology • psychology • therapeutic
             use*},
   Abstract = {RATIONALE: A few recent studies suggest that brain histamine
             levels and signaling via H(3) receptors play an important
             role in modulation of alcohol stimulation and reward in
             rodents. OBJECTIVE: The present study characterized the
             effects of a novel, selective, and brain penetrant H(3)
             receptor antagonist (JNJ-39220675) on the reinforcing
             effects of alcohol in rats. METHODS: The effect of
             JNJ-39220675 on alcohol intake and alcohol relapse-like
             behavior was evaluated in selectively bred
             alcohol-preferring (P) rats using the standard two-bottle
             choice method. The compound was also tested on operant
             alcohol self administration in non-dependent rats and on
             alcohol-induced ataxia using the rotarod apparatus. In
             addition, alcohol-induced dopamine release in the nucleus
             accumbens was tested in freely moving rats. RESULTS:
             Subcutaneous administration of the selective H(3) receptor
             antagonist dose-dependently reduced both alcohol intake and
             preference in alcohol-preferring rats. JNJ-39220675 also
             reduced alcohol preference in the same strain of rats
             following a 3-day alcohol deprivation. The compound
             significantly and dose-dependently reduced alcohol
             self-administration without changing saccharin
             self-administration in alcohol non-dependent rats.
             Furthermore, the compound did not change the ataxic effects
             of alcohol, alcohol elimination rate, nor alcohol-induced
             dopamine release in nucleus accumbens. CONCLUSIONS: These
             results indicate that blockade of H(3) receptor should be
             considered as a new attractive mechanism for the treatment
             of alcoholism.},
   Language = {eng},
   Doi = {10.1007/s00213-010-2092-4},
   Key = {fds275710}
}

@article{fds275593,
   Author = {Rezvani, AH and Overstreet, DH},
   Title = {Depressed-like behavior and alcohol drinking are co-morbid
             but independent in the fawn-hooded rats},
   Pages = {27-38},
   Year = {2010},
   Month = {December},
   Abstract = {The Fawn-Hooded (FH/Wjd) rat is an inbred strain that
             exhibits symptoms analogous to those exhibited by human
             depressives and alcoholics. The exaggerated swim test
             immobility and increased basal coticosterone levels are two
             of the depressed-like symptoms; importantly, these symptoms
             are reduced following chronic antidepressant treatments.
             Like alcoholics, the FH rat drinks excessive amounts of
             alcohol voluntarily that if allowed to continue will lead to
             tolerance and dependence, as revealed by anxiety-like
             behavior upon withdrawal of the alcohol. The human
             literature is inconclusive on how these two comorbid
             conditions are related; however, data in the animals clearly
             points to them being independent. Genetic studies (F1 and F2
             crosses, QTL) indicate no genetic overlap. Chronic treatment
             with antidepressants selectively reduces the depressed-like
             symptoms. Thus, the depressed-like behavior and excessive
             alcohol drinking appear to be independent traits in the
             FH/Wjd rat. © 2010 Nova Science Publishers, Inc. All rights
             reserved.},
   Key = {fds275593}
}

@article{fds275709,
   Author = {Rezvani, AH and Slade, S and Wells, C and Petro, A and Lumeng, L and Li,
             T-K and Xiao, Y and Brown, ML and Paige, MA and McDowell, BE and Rose, JE and Kellar, KJ and Levin, ED},
   Title = {Effects of sazetidine-A, a selective alpha4beta2 nicotinic
             acetylcholine receptor desensitizing agent on alcohol and
             nicotine self-administration in selectively bred
             alcohol-preferring (P) rats.},
   Journal = {Psychopharmacology},
   Volume = {211},
   Number = {2},
   Pages = {161-174},
   Year = {2010},
   Month = {August},
   ISSN = {1432-2072},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20535453},
   Keywords = {Animals • Azetidines • Dose-Response Relationship,
             Drug • Drug Administration Schedule • Ethanol
             • Male • Naltrexone • Narcotic Antagonists
             • Nicotine • Nicotinic Agonists • Pyridines
             • Rats • Receptors, Nicotinic • Reward •
             Saccharin • Self Administration • administration &
             dosage • administration & dosage* • metabolism*
             • pharmacology • pharmacology*},
   Abstract = {RATIONALE: Manipulations of nicotinic cholinergic receptors
             have been shown to influence both alcohol and nicotine
             intake. Sazetidine-A [6-(5(((S)-azetidine-2-yl)methoxy)pyridine-3-yl)hex-5-yn-1-ol]
             is a novel compound that potently and selectively
             desensitizes alpha4beta2 nicotinic receptors with only
             modest receptor activation. OBJECTIVES: The goal of the
             present study was to examine the effects of sazetidine-A on
             alcohol and nicotine self-administration in
             alcohol-preferring (P) rats. METHODS: P rats were given the
             choice of water or alcohol. Once stable baselines were
             established, the acute (0, 0.1, 0.3, 1, and 3 mg/kg, s.c.)
             and chronic (3 mg/kg for 10 days) effects of sazetidine-A on
             alcohol intake were assessed. Naltrexone (2.5 mg/kg) served
             as a positive control. The effect of sazetidine-A (3 mg/kg)
             and naltrexone (4 mg/kg) on saccharin (0.2%) preference was
             also assessed. In addition, the acute effects of
             sazetidine-A (3 mg/kg) and naltrexone (4 mg/kg) on alcohol
             intake after alcohol deprivation were evaluated. In another
             experiment, the effects of sazetidine-A (0, 1, or 3 mg/kg)
             on i.v. nicotine self-administration in P and NP rats were
             assessed. RESULTS: Sazetidine-A caused a dose-dependent
             reduction in alcohol intake. Chronic sazetidine-A also
             effectively reduced alcohol intake until the seventh day of
             treatment, when partial tolerance appeared to develop. In
             the post-deprivation study, sazetidine-A significantly
             reduced alcohol intake and preference. Sazetidine-A at 3
             mg/kg significantly reduced nicotine self-administration in
             both lines. CONCLUSIONS: Sazetidine-A significantly reduced
             alcohol and nicotine intake in P rats that self-administer
             higher levels of both drugs. Sazetidine-A may hold promise
             for the treatment of alcohol and nicotine
             addiction.},
   Language = {eng},
   Doi = {10.1007/s00213-010-1878-8},
   Key = {fds275709}
}

@article{fds275708,
   Author = {Rezvani, AH and Sexton, H and Levin, ED},
   Title = {Persistent high alcohol consumption in alcohol-preferring
             (P) rats results from a lack of normal aversion to
             alcohol.},
   Journal = {Alcohol and Alcoholism},
   Volume = {45},
   Number = {3},
   Pages = {219-222},
   Year = {2010},
   Month = {May},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20356869},
   Abstract = {AIMS: In this study, we tested the impact of pretreatment
             with alcohol on subsequent alcohol drinking in outbred
             Sprague-Dawley and selectively bred alcohol-preferring (P)
             rats. METHODS: As a pretreatment, male Sprague-Dawley and P
             rats were given a passive oral administration of either
             alcohol (1.0 g/kg) or tap water. Then, they were given free
             choice of drinking alcohol (5% v/v) or water in their home
             cages, which was measured over 4 weeks. RESULTS: Without
             alcohol pretreatment, there was no significant strain
             difference in alcohol preference; both strains preferred 5%
             (v/v) alcohol solution. The strain difference was only
             apparent in the groups given alcohol pretreatment. This
             arose from the fact that alcohol pretreatment significantly
             reduced alcohol preference in the Sprague-Dawley rats to a
             level well below 50%, while it did not alter drinking
             behavior in P rats. The same effects were seen with total
             alcohol consumption (g/kg/day). These effects persisted
             throughout the 4 weeks of the study. CONCLUSIONS: The
             principal difference between the Sprague-Dawley and P rats
             was that the P rats did not show the normal aversion to
             alcohol after forced exposure to alcohol that the
             Sprague-Dawley rats showed. One of the potential
             contributors to high alcohol intake and preference in P rats
             may be lack of sensitivity to aversive effects of
             alcohol.},
   Doi = {10.1093/alcalc/agq020},
   Key = {fds275708}
}

@article{fds216534,
   Author = {AH Rezvani and H Sexton and ED Levin},
   Title = {Persistent high alcohol consumption in alcohol-preferring
             (P) rats results from a lack of normal aversion to
             alcohol.},
   Journal = {Alcohol and alcoholism (Oxford, Oxfordshire)},
   Volume = {45},
   Number = {3},
   Pages = {219-22},
   Year = {2010},
   Month = {March},
   ISSN = {1464-3502},
   url = {http://dx.doi.org/10.1093/alcalc/agq020},
   Keywords = {Alcohol Drinking • Animals • Central Nervous
             System Depressants • Ethanol • Male •
             Motivation • Rats • Rats, Sprague-Dawley •
             Reward • Species Specificity • administration &
             dosage • genetics* • pharmacology •
             psychology*},
   Abstract = {OBJECTIVE: In this study, we tested the impact of
             pretreatment with alcohol on subsequent alcohol drinking in
             outbred Sprague-Dawley and selectively bred
             alcohol-preferring (P) rats. METHODS: As a pretreatment,
             male Sprague-Dawley and P rats were given a passive oral
             administration of either alcohol (1.0 g/kg) or tap water.
             Then, they were given free choice of drinking alcohol (5%
             v/v) or water in their home cages, which was measured over 4
             weeks. RESULTS: Without alcohol pretreatment, there was no
             significant strain difference in alcohol preference; both
             strains preferred 5% (v/v) alcohol solution. The strain
             difference was only apparent in the groups given alcohol
             pretreatment. This arose from the fact that alcohol
             pretreatment significantly reduced alcohol preference in the
             Sprague-Dawley rats to a level well below 50%, while it did
             not alter drinking behavior in P rats. The same effects were
             seen with total alcohol consumption (g/kg/day). These
             effects persisted throughout the 4 weeks of the study.
             CONCLUSIONS: The principal difference between the
             Sprague-Dawley and P rats was that the P rats did not show
             the normal aversion to alcohol after forced exposure to
             alcohol that the Sprague-Dawley rats showed. One of the
             potential contributors to high alcohol intake and preference
             in P rats may be lack of sensitivity to aversive effects of
             alcohol.},
   Language = {eng},
   Doi = {10.1093/alcalc/agq020},
   Key = {fds216534}
}

@article{fds275707,
   Author = {Levin, ED and Rezvani, AH and Xiao, Y and Slade, S and Cauley, M and Wells,
             C and Hampton, D and Petro, A and Rose, JE and Brown, ML and Paige, MA and McDowell, BE and Kellar, KJ},
   Title = {Sazetidine-A, a selective alpha4beta2 nicotinic receptor
             desensitizing agent and partial agonist, reduces nicotine
             self-administration in rats.},
   Journal = {Journal of Pharmacology and Experimental
             Therapeutics},
   Volume = {332},
   Number = {3},
   Pages = {933-939},
   Year = {2010},
   Month = {March},
   ISSN = {1521-0103},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20007754},
   Keywords = {Animals • Azetidines • Conditioning, Operant
             • Dose-Response Relationship, Drug • Drug Partial
             Agonism • Food • Male • Motivation •
             Motor Activity • Nicotine • Nicotinic Agonists
             • Pyridines • Rats • Rats, Sprague-Dawley
             • Receptors, Nicotinic • Self Administration
             • adverse effects • drug effects •
             pharmacology* • physiology*},
   Abstract = {Adequate treatment of tobacco addiction remains problematic.
             Part of the problem with treatment is a poor understanding
             of the pharmacologic aspects of nicotine contributing to
             addiction. In addition to activating nicotinic acetylcholine
             receptors, nicotine also desensitizes them. It is currently
             not known how much of each of nicotine's actions contribute
             to its particular behavioral effects. Sazetidine-A (saz-A)
             is a novel nicotinic receptor-desensitizing agent and
             partial agonist with high selectivity for alpha4beta2
             receptors. The current experiments were conducted to
             determine whether saz-A would reduce nicotine
             self-administration in rats and to characterize its
             ancillary effects. Adult male Sprague-Dawley rats were
             allowed to self-administer nicotine. After initial food
             pellet training followed by 10 sessions of nicotine
             self-administration training, the rats were administered
             saz-A (0.1-3 mg/kg s.c.) or the saline vehicle in a
             repeated-measures counterbalanced design. Saz-A at the 3
             mg/kg dose significantly decreased nicotine
             self-administration relative to performance of the same rats
             after saline injections. In a second study, long-term
             administration of this dose of sazetidine-A over the course
             of 10 sessions significantly reduced nicotine
             self-administration with no apparent diminution of effect.
             Saz-A in this dose range had only modest effects on
             locomotor activity, without any overall decrease in activity
             over a 1-h-long session. Saz-A significantly reduced food
             self-administration, but this effect was smaller than its
             effect on nicotine self-administration. Saz-A, which is a
             selective alpha4beta2-desensitizing agent and partial
             agonist, effectively reduces nicotine self-administration.
             This type of treatment holds promise for a new therapy to
             aid smoking cessation.},
   Language = {eng},
   Doi = {10.1124/jpet.109.162073},
   Key = {fds275707}
}

@article{fds275706,
   Author = {Rezvani, AH and Overstreet, DH and Vaidya, AH and Zhao, B and Levin,
             ED},
   Title = {Carisbamate, a novel antiepileptic candidate compound,
             attenuates alcohol intake in alcohol-preferring
             rats.},
   Journal = {Alcoholism: Clinical and Experimental Research},
   Volume = {33},
   Number = {8},
   Pages = {1366-1373},
   Year = {2009},
   Month = {August},
   ISSN = {1530-0277},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19413647},
   Keywords = {Administration, Oral • Alcohol Drinking • Animals
             • Anticonvulsants • Carbamates • Disease
             Models, Animal* • Dose-Response Relationship, Drug
             • Male • Rats • Time Factors •
             administration & dosage* • chemistry • genetics*
             • prevention & control*},
   Abstract = {BACKGROUND: Since 1994, when naltrexone (Revia) was approved
             by the FDA for the treatment of alcoholism, only 2 other
             drugs (Campral and Topamax have been approved for alcoholism
             treatment. However, various experimental drugs, including
             antiepileptic medications, have been tested in both animal
             models and in humans with some promising results. The
             purpose of this project was to study the effect of the novel
             neuromodulator carisbamate, which is in development for
             epilepsy treatment, on alcohol intake in selectively bred
             alcohol-preferring rats. METHODS: Male alcohol-preferring
             inbred P rats were allowed to freely drink water or alcohol
             (10%, v/v) using a 2-bottle choice procedure. After stable
             baselines for alcohol and water intakes were established,
             the acute effects of oral carisbamate (0, 10, 30, 45, 60,
             and 90 mg/kg) were assessed. Then, the chronic effect of the
             compound (60 mg/kg/day for 14 consecutive days) on alcohol
             intake was assessed in a separate group of male P rats. In
             another set of experiments, the effects of carisbamate and
             naltrexone on alcohol withdrawal-induced elevated drinking
             of alcohol, an index of craving, were compared. Rats were
             withdrawn from alcohol for 24 hours and were given vehicle,
             20 mg/kg naltrexone or 60 mg/kg carisbamate 30 minutes
             before re-exposure to alcohol. Alcohol and water intake was
             measured 6 hours after alcohol re-exposure. To determine the
             effects of carisbamate on saccharin preference, rats were
             put on a 2-bottle choice of water versus a solution of 2%
             saccharin. Then, the effect of the highest dose of
             carisbamate (90 mg/kg) and naltrexone (20 mg/kg) and the
             vehicle on saccharin preference was determined. RESULTS: Our
             results showed that there was a selective dose-dependent
             reduction in alcohol intake and preference in the
             alcohol-preferring P rat after an acute oral administration
             of carisbamate. There were no significant effects on food or
             water intake. Chronic administration of carisbamate
             significantly reduced alcohol intake and preference
             initially, but partial tolerance developed after the 10th
             treatment. The degree of tolerance development was less than
             that observed for naltrexone. Acute administration of
             carisbamate was more effective than naltrexone in reducing
             enhanced alcohol intake after a period of alcohol
             deprivation. Compared with control vehicle neither
             carisbamate nor naltrexone had a significant effect on
             saccharin intake and preference. CONCLUSION: The novel
             neuromodulator compound carisbamate has a favorable profile
             of effects on alcohol intake and related measures and should
             be considered for testing on human alcoholics.},
   Language = {eng},
   Doi = {10.1111/j.1530-0277.2009.00966.x},
   Key = {fds275706}
}

@article{fds275670,
   Author = {Tizabi, Y and Getachew, B and Rezvani, AH and Hauser, SR and Overstreet,
             DH},
   Title = {Antidepressant-like effects of nicotine and reduced
             nicotinic receptor binding in the Fawn-Hooded rat, an animal
             model of co-morbid depression and alcoholism.},
   Journal = {Progress in Neuro Psychopharmacology & Biological
             Psychiatry},
   Volume = {33},
   Number = {3},
   Pages = {398-402},
   Year = {2009},
   Month = {April},
   ISSN = {0278-5846},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18835320},
   Keywords = {Alcoholism • Alkaloids • Analysis of Variance
             • Animals • Antidepressive Agents • Azocines
             • Depression • Disease Models, Animal • Drug
             Administration Schedule • Male • Nicotine •
             Protein Binding • Quinolizines • Rats • Rats,
             Inbred Strains • Receptors, Nicotinic • Swimming
             • Tritium • complications • drug effects
             • drug therapy* • genetics • metabolism
             • metabolism* • pathology • pharmacology
             • therapeutic use*},
   Abstract = {A strong positive association between depression and
             alcoholism is evident in epidemiological studies. Curiously,
             the incidence of smoking (nicotine intake) is also very high
             among depressed individuals. Because neuronal nicotinic
             receptors have been implicated in mood regulation as well as
             in reinforcing effects of alcohol, it was of interest to
             determine whether inherent changes in these receptors may be
             manifested in an animal model that expresses both
             depressive-like characteristics and high alcohol intake.
             Thus, Fawn-Hooded (FH) rats along with their control ACI
             rats were used to measure the density of the high affinity
             nicotinic receptor in discrete brain regions. Furthermore,
             the effects of acute and chronic nicotine on depressive-like
             characteristics of FH rats were also evaluated. Measurements
             of [(3)H]cytisine binding (selective for alpha4beta2
             nicotinic receptor subtype) revealed a reduction in these
             receptors only in the striatum of FH rats, a result very
             similar to that observed in selectively-bred
             alcohol-preferring (P) rats. Administration of nicotine
             acutely (0.4 mg/kg, sc) resulted in a significant reduction
             of immobility in the forced swim test (FST) in FH rats only,
             implying an antidepressant-like effect of nicotine. Another
             group of FH rats were administered 0.4 mg/kg nicotine
             (daily, sc) for 14 days and their behavior in the FST was
             evaluated 22-24 h after the last injection. In this case,
             nicotine also had a significant antidepressant-like effect
             in FH rats suggesting no tolerance to nicotine had occurred.
             The effects of nicotine on FST behavior are very similar to
             those observed in Flinders Sensitive Line rats, a putative
             animal model of depression. Together, these findings provide
             additional evidence for antidepressant-like effects of
             nicotine and strengthen the postulated association between
             striatal nicotinic receptors and high alcohol intake. Thus,
             nicotinic receptors could be suitable targets for the
             development of novel pharmacotherapy for treatment of
             depression and possibly alcoholism.},
   Language = {eng},
   Doi = {10.1016/j.pnpbp.2008.09.010},
   Key = {fds275670}
}

@article{fds275705,
   Author = {Rezvani, AH and Kholdebarin, E and Brucato, FH and Callahan, PM and Lowe, DA and Levin, ED},
   Title = {Effect of R3487/MEM3454, a novel nicotinic alpha7 receptor
             partial agonist and 5-HT3 antagonist on sustained attention
             in rats.},
   Journal = {Progress in Neuro Psychopharmacology & Biological
             Psychiatry},
   Volume = {33},
   Number = {2},
   Pages = {269-275},
   Year = {2009},
   Month = {March},
   ISSN = {0278-5846},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19110025},
   Keywords = {Animals • Attention • Conditioning, Operant •
             Dose-Response Relationship, Drug • Female •
             Galantamine • Nicotinic Agonists • Nootropic
             Agents • Psychomotor Performance • Rats •
             Rats, Sprague-Dawley • Receptors, Nicotinic •
             Serotonin 5-HT3 Receptor Antagonists* • Serotonin
             Antagonists • Signal Detection, Psychological •
             drug effects • drug effects* • pharmacology •
             pharmacology*},
   Abstract = {It is well established that nicotinic systems in the brain
             are critically involved in attentional processes in both
             animals and humans. The current study assessed the effects
             of a novel nicotinic alpha7 receptor partial agonist and
             5-HT3 antagonist, R3487/MEM3454 (also referred to as R3487
             or MEM 3454) on sustained attention in rats performing an
             operant visual signal detection task. The effects of
             R3487/MEM3454 were compared to those of the
             acetylcholinesterase inhibitor/nicotinic alpha7 allosteric
             positive modulator galanthamine. Adult female Sprague-Dawley
             rats were injected subcutaneously with R3487/MEM3454 (0.03,
             0.1, 0.15, 0.3 and 0.6 mg/kg), galanthamine (0.25, 0.5, 1, 2
             mg/kg) or vehicle 30 min before the attentional test. In the
             second study, the time-dependent effects of R3487/MEM3454
             were assessed by injecting the compound (0.6 mg/kg, s.c.) at
             different pretreatment intervals (30, 60 or 90 min) before
             the start of the attentional task. Our results show a
             significant dose-effect for R3487/MEM3454 on percent hit
             accuracy performance without any significant alteration on
             percent correct rejection performance. In the time-dependent
             test, R3487/MEM3454 significantly increased the percent hit
             accuracy performance when animals were injected 60 min
             before the start of the attentional task. Administration of
             galanthamine failed to significantly increase percent hit
             accuracy performance and increasing the dose of galanthamine
             produced a decrease in percent correct rejection
             performance. The present findings with R3487/MEM3454 suggest
             that nicotinic alpha7 receptors and/or 5-HT3 receptors may
             play an important role in modulating sustained attention and
             that R3487/MEM3454 may have therapeutic potential in
             improving sustained attention in humans.},
   Language = {eng},
   Doi = {10.1016/j.pnpbp.2008.11.018},
   Key = {fds275705}
}

@article{fds275704,
   Author = {Rezvani, AH and Kholdebarin, E and Cauley, MC and Dawson, E and Levin,
             ED},
   Title = {Attenuation of pharmacologically-induced attentional
             impairment by methylphenidate in rats.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {92},
   Number = {1},
   Pages = {141-146},
   Year = {2009},
   Month = {March},
   ISSN = {0091-3057},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19041337},
   Keywords = {Animals • Attention • Central Nervous System
             Stimulants • Dizocilpine Maleate • Excitatory
             Amino Acid Antagonists • Female • Mecamylamine
             • Methylphenidate • Muscarinic Antagonists •
             Nicotinic Antagonists • Photic Stimulation •
             Psychomotor Performance • Rats • Rats,
             Sprague-Dawley • Receptors, N-Methyl-D-Aspartate •
             Scopolamine Hydrobromide • Signal Detection,
             Psychological • Visual Perception • antagonists &
             inhibitors • drug effects • drug effects* •
             pharmacology • pharmacology*},
   Abstract = {Methylphenidate is widely used as a treatment option for
             attention deficit hyperactivity disorder. In animal models
             of attentional impairment, it is an important validation to
             determine whether this clinically effective treatment
             attenuates deficits. The purpose of the current study was to
             determine whether methylphenidate can diminish attentional
             impairment induced by three pharmacological agents with
             different mechanisms of action: scopolamine, mecamylamine,
             and dizocilpine. Female rats were trained on an operant
             visual signal detection task. Ten min before the test, the
             rats were injected subcutaneously with methylphenidate (0,
             0.1, 0.3 mg/kg), scopolamine (0, 0.005, 0.01 mg/kg),
             mecamylamine (0, 2, 4 mg/kg), dizocilpine (0, 0.025, 0.05
             mg/kg) or combinations of methylphenidate with these drugs.
             In each of the experiments, all rats received every
             treatment in a repeated measures counterbalanced order.
             Correction rejection accuracy was impaired by all three of
             the antagonists and these effects were attenuated by
             methylphenidate. Both scopolamine at 0.01 and dizocilpine at
             0.05 mg/kg significantly impaired percent correct rejection
             choice accuracy, an effect that was ameliorated by
             methylphenidate. Mecamylamine (4 mg/kg) impaired attentional
             performance by reducing percent hit and percent correct
             rejection. Co-administration of methylphenidate failed to
             significantly affect the mecamylamine-induced attentional
             impairment. Methylphenidate alone at 0.3 mg/kg significantly
             improved percent hit choice accuracy only in low-performing
             rats in one experiment, an effect which was reversed by
             scopolamine. These data show that methylphenidate
             effectively reverses the attentional impairment caused by
             scopolamine and dizocilpine. These findings further validate
             the operant visual signal detection task for assessing
             attentional impairments and their reversal.},
   Language = {eng},
   Doi = {10.1016/j.pbb.2008.11.005},
   Key = {fds275704}
}

@article{fds275703,
   Author = {Levin, ED and Petro, A and Rezvani, AH and Pollard, N and Christopher,
             NC and Strauss, M and Avery, J and Nicholson, J and Rose,
             JE},
   Title = {Nicotinic alpha7- or beta2-containing receptor knockout:
             effects on radial-arm maze learning and long-term nicotine
             consumption in mice.},
   Journal = {Behavioural Brain Research},
   Volume = {196},
   Number = {2},
   Pages = {207-213},
   Year = {2009},
   Month = {January},
   ISSN = {1872-7549},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18831991},
   Keywords = {Animals • Female • Genotype • Male •
             Maze Learning • Mice • Mice, Inbred C57BL •
             Mice, Knockout • Nicotine • Nicotinic Agonists
             • Psychomotor Performance • Receptors, Nicotinic
             • Self Administration • Sex Characteristics •
             Tobacco Use Disorder • administration & dosage •
             drug effects • genetics • genetics* •
             pharmacology • physiology • physiology* •
             psychology*},
   Abstract = {Classically, it has been thought that high-affinity
             nicotinic receptors-containing beta2 subunits are the most
             important receptor subtypes for nicotinic involvement in
             cognitive function and nicotine self-administration, while
             low affinity alpha7-containing nicotinic receptors have not
             been thought to be important. In the current study, we found
             that knockout of either beta2 or alpha7 subunits caused
             significant deficits in spatial discrimination in mice. The
             character of the impairment in the two knockouts was
             different. The beta2 knockout preferentially impaired
             cognition in males while the alpha7 caused impairment
             regardless of sex. Both beta2- and alpha7-containing
             nicotinic receptors also are important for nicotine
             self-administration, also in different ways. Most animal
             model studies of nicotine self-administration are relatively
             short-term whereas the problem of tobacco addiction is
             considerably longer-term. To better model the impact of
             nicotinic receptor subtypes on nicotine self-administration
             over the long-term, we studied the impact of genetic
             knockout of low affinity alpha7 receptors vs. high-affinity
             beta2-containing nicotinic receptors. Mice with knockouts of
             either of these receptors and their wildtype counter parts
             were given free access to a choice of nicotine-containing
             and nicotine-free solution in their home cages on a
             continuous basis over a period of 5 months. During the first
             few weeks, the beta2-containing nicotinic receptor knockout
             mice showed a significant decrease in nicotine consumption
             relative to wildtype mice, whereas the alpha7 knockout mice
             did not significantly differ from wildtype controls at the
             beginning of their access to nicotine. Interestingly, in the
             longer-term after the first few weeks of nicotine access,
             the beta2 knockout mice returned to wildtype mouse levels of
             nicotine consumption, whereas the alpha7 knockout mice
             developed an emergent decrease in nicotine consumption. The
             alpha7 receptor knockout-induced decrease in nicotine
             consumption persisted for the 5-month period of the study.
             Both alpha7- and beta2-containing nicotinic receptors play
             critical roles in cognitive function and nicotine
             self-administration. Regarding cognitive function,
             beta2-containing receptors are important for maintaining
             normal sex differences in spatial learning and memory,
             whereas alpha7 receptors are important for cognitive
             function regardless of sex. Regarding nicotine
             self-administration high-affinity beta2-containing nicotinic
             receptors are important for consumption during the initial
             phase of nicotine access, but it is the alpha7 nicotinic
             receptors that are important for the longer-term regulation
             of nicotine consumption.},
   Language = {eng},
   Doi = {10.1016/j.bbr.2008.08.048},
   Key = {fds275703}
}

@article{fds275702,
   Author = {Levin, ED and Slade, S and Johnson, M and Petro, A and Horton, K and Williams, P and Rezvani, AH and Rose, JE},
   Title = {Ketanserin, a 5-HT2 receptor antagonist, decreases nicotine
             self-administration in rats.},
   Journal = {European Journal of Pharmacology},
   Volume = {600},
   Number = {1-3},
   Pages = {93-97},
   Year = {2008},
   Month = {December},
   ISSN = {1879-0712},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18950618},
   Keywords = {Animals • Behavior, Animal • Dose-Response
             Relationship, Drug • Drug Administration Schedule
             • Ketanserin • Male • Nicotine •
             Nicotinic Agonists • Rats • Rats, Sprague-Dawley
             • Self Administration • Serotonin • Serotonin
             5-HT2 Receptor Antagonists* • Serotonin Antagonists
             • Tobacco Use Disorder • administration & dosage
             • administration & dosage* • drug effects •
             drug therapy • metabolism • pharmacology •
             pharmacology* • physiopathology},
   Abstract = {Nicotine intake constitutes a principal mechanism for
             tobacco addiction. In addition to primary effects on
             nicotinic acetylcholine receptors, nicotine has cascading
             effects, which may also underlie its neurobehavioral
             actions. Nicotine induces serotonin (5-HT) release, which
             has not classically been thought to be involved in tobacco
             addiction as dopamine has. However, addiction can be
             characterized more as a disorder of compulsion than a
             disorder of enjoyment. 5-HT mechanisms play key roles in
             compulsive disorders. Nicotine-induced 5-HT release may be a
             key to tobacco addiction. Ketanserin, a 5-HT2a and 5-HT2c
             receptor antagonist, significantly attenuates nicotine
             effects on attention and memory. These studies were
             conducted to determine if ketanserin would reduce nicotine
             self-administration in rats. Male Sprague-Dawley rats (N=12)
             were given initial food pellet training and then 10 sessions
             of nicotine self-administration training (0.03
             mg/kg/infusion, i.v.). Then the rats were administered
             ketanserin (1 or 2 mg/kg, s.c.) or the saline vehicle.
             Ketanserin (2 mg/kg) significantly decreased nicotine
             self-administration. This did not seem to be due to sedative
             or amnestic effects of ketanserin. In a second study, the
             effects of repeated administration of 2 mg/kg ketanserin
             (N=11) vs. saline injections (N=10) were examined. In the
             initial phase, the acute effectiveness of ketanserin in
             significantly reducing nicotine self-administration was
             replicated. The effect became attenuated during the
             following several sessions, but the significant effect
             became re-established during the final phases of this
             two-week study. 5-HT mechanisms play critical roles in the
             maintenance of nicotine self-administration. Better
             understanding of those roles may help lead to new 5-HT-based
             treatments for tobacco addiction.},
   Language = {eng},
   Doi = {10.1016/j.ejphar.2008.10.016},
   Key = {fds275702}
}

@article{fds275699,
   Author = {Morey, JS and Ryan, JC and Bottein Dechraoui and M-Y and Rezvani, AH and Levin, ED and Gordon, CJ and Ramsdell, JS and Van Dolah,
             FM},
   Title = {Liver genomic responses to ciguatoxin: evidence for
             activation of phase I and phase II detoxification pathways
             following an acute hypothermic response in
             mice.},
   Journal = {Toxicological Sciences},
   Volume = {103},
   Number = {2},
   Pages = {298-310},
   Year = {2008},
   Month = {June},
   ISSN = {1096-0929},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18353800},
   Keywords = {Animals • Body Temperature • Body Temperature
             Regulation • Ciguatera Poisoning • Ciguatoxins
             • Cytochrome P-450 Enzyme System • Down-Regulation
             • Genomics • Glutathione Transferase • Liver
             • Metabolic Detoxication, Phase I • Metabolic
             Detoxication, Phase II • Mice • Oligonucleotide
             Array Sequence Analysis • Poisons • RNA, Messenger
             • Transcription, Genetic • analysis •
             biosynthesis • chemistry • drug effects •
             drug effects* • enzymology • genetics •
             genetics* • metabolism • toxicity*},
   Abstract = {Ciguatoxins (CTX) are polyether neurotoxins that target
             voltage-gated sodium channels and are responsible for
             ciguatera, the most common fish-borne food poisoning in
             humans. This study characterizes the global transcriptional
             response of mouse liver to a symptomatic dose (0.26 ng/g) of
             the highly potent Pacific ciguatoxin-1 (P-CTX-1). At 1 h
             post-exposure 2.4% of features on a 44K whole genome array
             were differentially expressed (p < or = 0.0001), increasing
             to 5.2% at 4 h and decreasing to 1.4% by 24 h post-CTX
             exposure. Data were filtered (/fold change/ > or = 1.5 and p
             < or = 0.0001 in at least one time point) and a trend set of
             1550 genes were used for further analysis. Early gene
             expression was likely influenced prominently by an acute 4
             degrees C decline in core body temperature by 1 h, which
             resolved by 8 h following exposure. An initial
             downregulation of 32 different solute carriers, many
             involved in sodium transport, was observed. Differential
             gene expression in pathways involving eicosanoid
             biosynthesis and cholesterol homeostasis was also noted.
             Cytochrome P450s (Cyps) were of particular interest due to
             their role in xenobiotic metabolism. Twenty-seven genes,
             mostly members of Cyp2 and Cyp4 families, showed significant
             changes in expression. Many Cyps underwent an initial
             downregulation at 1 h but were quickly and strongly
             upregulated at 4 and 24 h post-exposure. In addition to
             Cyps, increases in several glutathione S-transferases were
             observed, an indication that both phase I and phase II
             metabolic reactions are involved in the hepatic response to
             CTX in mice.},
   Language = {eng},
   Doi = {10.1093/toxsci/kfn055},
   Key = {fds275699}
}

@article{fds275701,
   Author = {Rezvani, AH and Eddins, D and Slade, S and Hampton, DS and Christopher,
             NC and Petro, A and Horton, K and Johnson, M and Levin,
             ED},
   Title = {Neonatal 6-hydroxydopamine lesions of the frontal cortex in
             rats: persisting effects on locomotor activity, learning and
             nicotine self-administration.},
   Journal = {Neuroscience},
   Volume = {154},
   Number = {3},
   Pages = {885-897},
   Year = {2008},
   Month = {June},
   ISSN = {0306-4522},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18511204},
   Keywords = {Animals • Animals, Newborn • Brain Chemistry
             • Chromatography, High Pressure Liquid • Dopamine
             • Female • Learning • Male • Maze
             Learning • Memory • Motor Activity • Nicotine
             • Nicotinic Agonists • Norepinephrine •
             Oxidopamine* • Prefrontal Cortex • Rats •
             Rats, Sprague-Dawley • Self Administration •
             Serotonin • Sympathectomy, Chemical* •
             Sympatholytics* • Tobacco Use Disorder •
             administration & dosage • drug effects • drug
             effects* • metabolism • pharmacology* •
             physiology • physiology* • psychology*},
   Abstract = {Dopaminergic innervation of the frontal cortex in adults is
             important for a variety of cognitive functions and
             behavioral control. However, the role of frontal cortical
             dopaminergic innervation for neurobehavioral development has
             received little attention. In the current study, rats were
             given dopaminergic lesions in the frontal cortex with local
             micro-infusions of 6-hydroxydopamine (6-OHDA) at 1 week of
             age. The long-term behavioral effects of neonatal frontal
             cortical 6-OHDA lesions were assessed in a series of tests
             of locomotor activity, spatial learning and memory, and i.v.
             nicotine self-administration. In addition, neurochemical
             indices were assessed with tissue homogenization and HPLC in
             the frontal cortex, striatum, and nucleus accumbens of
             neonatal and adult rats after neonatal 6-OHDA lesions. In
             neonatal rats, frontal 6-OHDA lesions as intended caused a
             significant reduction in frontal cortical dopamine without
             effects on frontal cortical 5-HT and norepinephrine. The
             frontal cortical dopamine depletion increased 5-HT and
             norepinephrine levels in the nucleus accumbens. Locomotor
             activity assessment during adulthood in the figure-8 maze
             showed that lesioned male rats were hyperactive relative to
             sham-lesioned males. Locomotor activity of female rats was
             not significantly affected by the neonatal frontal 6-OHDA
             lesion. Learning and memory in the radial-arm maze was also
             affected by neonatal frontal 6-OHDA lesions. There was a
             general trend toward impaired performance in early maze
             acquisition and a paradoxical improvement at the end of
             cognitive testing. Nicotine self-administration showed
             significant lesion x sex interactions. The sex difference in
             nicotine self-administration with females self-administering
             significantly more nicotine than males was reversed by
             neonatal 6-OHDA frontal cortical lesions. Neurochemical
             studies in adult rats showed that frontal cortical dopamine
             and DOPAC levels significantly correlated with nicotine
             self-administration in the 6-OHDA-lesioned animals but not
             in the controls. Frontal cortical 5-HT and 5HIAA showed
             inverse correlations with nicotine self-administration in
             the 6-OHDA-lesioned animals but not in the controls. These
             results show that interfering with normal dopamine
             innervation of the frontal cortex during early postnatal
             development has persisting behavioral effects, which are
             sex-specific.},
   Language = {eng},
   Doi = {10.1016/j.neuroscience.2008.04.020},
   Key = {fds275701}
}

@article{fds275700,
   Author = {Rezvani, AH and Tizabi, Y and Getachew, B and Hauser, SR and Caldwell,
             DP and Hunter, C and Levin, ED},
   Title = {Chronic nicotine and dizocilpine effects on nicotinic and
             NMDA glutamatergic receptor regulation: interactions with
             clozapine actions and attentional performance in
             rats.},
   Journal = {Progress in Neuro Psychopharmacology & Biological
             Psychiatry},
   Volume = {32},
   Number = {4},
   Pages = {1030-1040},
   Year = {2008},
   Month = {May},
   ISSN = {0278-5846},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18343006},
   Keywords = {Alkaloids • Animals • Antipsychotic Agents •
             Attention • Azocines • Brain Chemistry •
             Bungarotoxins • Clozapine • Dizocilpine Maleate
             • Dose-Response Relationship, Drug • Excitatory
             Amino Acid Antagonists • Female • Nicotine •
             Nicotinic Agonists • Psychomotor Performance •
             Quinolizines • Rats • Rats, Sprague-Dawley •
             Receptors, N-Methyl-D-Aspartate • Receptors, Nicotinic
             • Signal Detection, Psychological • drug effects
             • drug effects* • metabolism •
             pharmacology*},
   Abstract = {Blockade of NMDA glutamate receptors with dizocilpine
             (MK-801) has been shown to cause substantial cognitive
             deficits and has been used to model symptoms of
             schizophrenia. Nicotine or nicotinic agonists, in contrast,
             may enhance cognitive or attentional functions and be of
             therapeutic potential in schizophrenia. Nicotinic-glutamatergic
             interactions, therefore, may have important implications in
             cognitive functions and antipsychotic treatments. Clozapine,
             a widely used antipsychotic drug, has been shown in some
             studies to be effective in ameliorating the cognitive
             deficits associated with schizophrenia. However, there is
             some evidence to suggest that clozapine similar to
             haloperidol may impair sustained attention in rats. In this
             study, we sought to determine whether chronic nicotine or
             dizocilpine may modify the effects of acute clozapine on
             attentional parameters and whether the behavioral effects
             would correlate with nicotinic or NMDA receptor densities in
             discrete brain regions. Adult female rats trained on an
             operant visual signal detection task were given 4 weeks of
             nicotine (5 mg/kg/day), dizocilpine (0.15 mg/kg/day), the
             same doses of both nicotine and dizocilpine as a mixture, or
             saline by osmotic minipump. While on chronic treatment, rats
             received acute injections of various doses of clozapine (0,
             0.625, 1.25, 2.5 mg/kg, sc) 10 min prior to tests on
             attentional tasks. The pumps were removed on day 28 and 24 h
             later the animals were sacrificed for measurements of
             receptor densities in specific brain regions. The percent
             correct hit as a measure of sustained attention was
             significantly impaired by clozapine in a dose-related
             manner. Neither chronic nicotine nor dizocilpine affected
             this measure on their own or modified the effects of
             clozapine. Both nicotine and dizocilpine affected the
             receptor bindings in a region specific manner and their
             combination further modified the effects of each other in
             selective regions. Attentional performance was inversely
             correlated with alpha-bungarotoxin binding in the frontal
             cortex only. In conclusion, the data suggest attentional
             impairments with clozapine alone and no modification of this
             effect with nicotine or dizocilpine. Moreover, cortical low
             affinity nicotinic receptors may have a role in attentional
             functions.},
   Language = {eng},
   Doi = {10.1016/j.pnpbp.2008.01.018},
   Key = {fds275700}
}

@article{fds275721,
   Author = {Schramm-Sapyta, NL and Kingsley, MA and Rezvani, AH and Propst, K and Swartzwelder, HS and Kuhn, CM},
   Title = {Early ethanol consumption predicts relapse-like behavior in
             adolescent male rats.},
   Journal = {Alcoholism, Clinical and Experimental Research},
   Volume = {32},
   Number = {5},
   Pages = {754-762},
   Year = {2008},
   Month = {May},
   ISSN = {1530-0277},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18336637},
   Keywords = {Alcohol Drinking • Animals • Anxiety • Choice
             Behavior • Corticosterone • Exploratory Behavior
             • Male • Models, Animal • Phenotype •
             Rats • Rats, Sprague-Dawley • Recurrence •
             epidemiology* • metabolism • physiology •
             physiopathology},
   Abstract = {Alcohol abuse disorders emerge over time with repeated
             consumption of ethanol, but not all ethanol drinkers develop
             these disorders. There are pre-existing characteristics that
             indicate which drinkers are most likely to abuse alcohol.
             Adolescence, novelty seeking, and high stress reactivity are
             among the characteristics of the most vulnerable
             individuals. In addition, an individual's response to his or
             her first exposure to the drug influences future
             consumption. We assessed an array of behavioral and hormonal
             characteristics in adolescent (28-day-old) male rats before
             exposure to ethanol, and then determined which rats were
             most prone to high levels of alcohol drinking.The
             assessments consisted of measures of anxiety (elevated plus
             maze), response to novelty (open field locomotion, novel
             object exploration), and circulating corticosterone levels
             after mild restraint and after the elevated plus maze task.
             After this test battery, the rats were placed in lickometer
             cages nightly (5 pm to 9 am) for evaluation of fluid
             consumption. Rats were first habituated to the cages with
             water in the lickometer bottles, and then given 10% (v/v)
             ethanol for 3 nights as the only available fluid. After this
             forced ethanol exposure, the rats were allowed to choose
             between 8% ethanol and water for 10 consecutive nights.
             After 2 nights of abstinence, the rats were again placed in
             the lickometer cages and given a choice between 8% ethanol
             and water to assess ethanol consumption in response to
             alcohol deprivation, a measure of relapse-like
             behavior.Ethanol consumption on the third day of forced
             consumption was significantly correlated with ethanol
             consumption on days 8 to 10 of the choice phase, which in
             turn was significantly correlated to relapse-like
             consumption. Preference for ethanol was also significantly
             correlated with early consumption. Novel object exploration,
             open field activity, open arm time in the elevated plus
             maze, initial water consumption, and circulating
             corticosterone levels did not significantly predict
             deprivation-stimulated consumption.These results suggest
             that consumption during early exposure to ethanol
             establishes a pattern leading to development of increased
             alcohol consumption and preference in adolescent male rats.
             In addition, they represent an animal model of the
             well-described observation that humans who consume large
             quantities of ethanol during early exposure are the most
             likely to repeat heave drinking behavior. Furthermore, early
             consumption is distinct from novelty seeking, anxiety, and
             stress hormone levels which are also thought to contribute
             to vulnerability to alcoholism.},
   Language = {eng},
   Doi = {10.1111/j.1530-0277.2008.00631.x},
   Key = {fds275721}
}

@article{fds275698,
   Author = {Bottein Dechraoui and M-Y and Rezvani, AH and Gordon, CJ and Levin, ED and Ramsdell, JS},
   Title = {Repeat exposure to ciguatoxin leads to enhanced and
             sustained thermoregulatory, pain threshold and motor
             activity responses in mice: relationship to blood ciguatoxin
             concentrations.},
   Journal = {Toxicology},
   Volume = {246},
   Number = {1},
   Pages = {55-62},
   Year = {2008},
   Month = {April},
   ISSN = {0300-483X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18280027},
   Keywords = {Animals • Body Temperature • Body Temperature
             Regulation • Body Weight • Cell Survival •
             Ciguatoxins • Male • Mice • Mice, Inbred
             C57BL • Motor Activity • Pain Measurement •
             Poisons • administration & dosage • blood •
             blood* • drug effects • drug effects* •
             methods • toxicity*},
   Abstract = {Ciguatera is a common illness in tropical and subtropical
             regions that manifests in complex and long-lived symptoms
             which are more severe in subsequent exposures. This study
             measures central and peripheral neurologic signs, in
             parallel with blood toxin levels, in mice exposed once or
             twice (at 3 days interval) to a sublethal dose of ciguatoxin
             P-CTX-1 (0.26ng/g via i.p.). Mice were implanted with
             radiotransmitters to monitor motor activity and core
             temperature. A single exposure to ciguatoxin elicited an
             immediate and transient decrease in motor activity and
             temperature, and subsequent long-lasting thermoregulatory
             dysfunction resulting in stabilized body temperature around
             36.0 degrees C with no observable circadian rhythm. The
             hypothermic response and the reduced activity were enhanced
             with a second exposure with 30% of the mice dying within 7h.
             Measurement of the peripheral nervous system by the tail
             flick assay revealed increased latency with a single
             ciguatoxin exposure, and a greater effect following the
             second exposure. Toxin was measurable in blood up to 3 days
             following the first exposure; at the 1h time point the
             concentrations were significantly elevated after a second
             exposure. These findings indicate an early response to
             ciguatoxin manifest in a central response to lower body
             temperature and reduce motor activity and a more persistent
             effect on the peripheral system leading to spinal heat
             antinociception and delayed fever-like response. The greater
             neurological response to a second ciguatoxin exposure was
             associated with elevated concentrations of ciguatoxin in the
             blood solely over the first hour of exposure. In conclusion,
             a single exposure to toxin exerts a significant neurological
             response which may be enhanced with subsequent
             exposure.},
   Language = {eng},
   Doi = {10.1016/j.tox.2007.12.013},
   Key = {fds275698}
}

@article{fds275697,
   Author = {Rezvani, AH and Kholdebarin, E and Dawson, E and Levin,
             ED},
   Title = {Nicotine and clozapine effects on attentional performance
             impaired by the NMDA antagonist dizocilpine in female
             rats.},
   Journal = {The International Journal of Neuropsychopharmacology},
   Volume = {11},
   Number = {1},
   Pages = {63-70},
   Year = {2008},
   Month = {February},
   ISSN = {1461-1457},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17295931},
   Keywords = {Animals • Antipsychotic Agents • Attention •
             Clozapine • Conditioning, Operant • Dizocilpine
             Maleate • Dose-Response Relationship, Drug •
             Excitatory Amino Acid Antagonists • Female •
             Nicotine • Nicotinic Agonists • Photic Stimulation
             • Psychomotor Performance • Rats • Rats,
             Sprague-Dawley • Signal Detection, Psychological •
             antagonists & inhibitors* • drug effects • drug
             effects* • pharmacology*},
   Abstract = {Cognitive impairment is very prevalent in schizophrenia and
             is currently undertreated in most patients. Attentional
             deficit is one of the hallmark symptoms of schizophrenia.
             Antipsychotic drugs, which can be quite effective in
             combating hallucinations are often ineffective in reducing
             cognitive impairment and can potentiate cognitive
             impairment. Previously, we found that the antipsychotic drug
             clozapine impaired, while nicotine improved, the accuracy of
             rats performing a visual signal detection attentional task
             in normal rats. For the current study, in a model of
             cognitive impairment of schizophrenia with the NMDA
             antagonist dizocilpine (0.05 mg/kg), we examined the effects
             of clozapine and nicotine on significantly impaired
             attentional hit accuracy. This dizocilpine-induced
             impairment was significantly (p<0.05) reversed by either
             clozapine (1.25 mg/kg) or nicotine (0.025 mg/kg).
             Interestingly, when clozapine and nicotine were given
             together, they blocked each other's beneficial effects. When
             the effective doses of 1.25 mg/kg clozapine and 0.025 mg/kg
             nicotine were given together the combination no longer
             significantly reversed the dizocilpine-induced hit-accuracy
             impairment. Given that the great majority of people with
             schizophrenia smoke, the potential beneficial effects of
             clozapine on attentional function may be largely blocked by
             self-administered nicotine. In addition, there are promising
             results concerning the development of nicotinic treatments
             to reverse cognitive deficits including attentional
             impairment. This is supported in the current study by the
             reversal of the dizocilpine-induced attentional impairment
             by nicotine. However, in schizophrenia the efficacy of
             nicotinic treatments may be limited by co-treatment with
             antipsychotic drugs like clozapine. It will be important to
             determine which of the complex effects of clozapine and
             nicotine are key in reversing attentional impairment and how
             they block each other's effects for the development of
             therapy to combat the attentional impairment of
             schizophrenia.},
   Language = {eng},
   Doi = {10.1017/S1461145706007528},
   Key = {fds275697}
}

@article{fds275696,
   Author = {Levin, ED and Rezvani, AH},
   Title = {Nicotinic interactions with antipsychotic drugs, models of
             schizophrenia and impacts on cognitive function.},
   Journal = {Biochemical Pharmacology},
   Volume = {74},
   Number = {8},
   Pages = {1182-1191},
   Year = {2007},
   Month = {October},
   ISSN = {0006-2952},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17714691},
   Keywords = {Animals • Antipsychotic Agents • Cognition •
             Cognition Disorders • Drug Interactions • Humans
             • Nicotine • Receptors, Nicotinic •
             Schizophrenia • drug effects* • drug therapy
             • drug therapy* • etiology • pharmacology*
             • physiology • therapeutic use},
   Abstract = {People with schizophrenia often have substantial cognitive
             impairments, which may be related to nicotinic receptor
             deficits, (alpha7 and alpha4beta2), documented in the brains
             of people with schizophrenia. The large majority of people
             with schizophrenia smoke cigarettes. Thus, nicotinic
             interactions with antipsychotic drugs are widespread.
             Complementary co-therapies of novel nicotinic ligands are
             being developed to add to antipsychotic therapy to treat the
             cognitive impairment of schizophrenia. Thus, it is critical
             to understand the interaction between nicotinic treatments
             and antipsychotic drugs. Nicotinic interactions with
             antipsychotic drugs, are complex since both nicotine and
             antipsychotics have complex actions. Nicotine stimulates and
             desensitizes nicotinic receptors of various subtypes and
             potentiates the release of different neurotransmitters.
             Antipsychotics also act on a verity of receptor systems. For
             example, clozapine acts as an antagonist at a variety of
             neurotransmitter receptors such as those for dopamine,
             serotonin, norepinepherine and histamine. In a series of
             studies, we have found that in normally functioning rats,
             moderate doses of clozapine impair working memory and that
             clozapine blocks nicotine-induced memory and attentional
             improvement. Clozapine and nicotine can attenuate each
             other's beneficial effects in reversing the memory
             impairment caused by the psychototmimetic drug dizocilpine.
             A key to the clozapine-induced attenuation of
             nicotine-induced cognitive improvement appears to be its
             5HT(2) antagonist properties. The selective 5HT(2)
             antagonist ketanserin has a similar action of blocking
             nicotine-induced memory and attentional improvements. It is
             important to consider the interactions between nicotinic and
             antipsychotic drugs to develop the most efficacious
             treatment for cognitive improvement in people with
             schizophrenia.},
   Language = {eng},
   Doi = {10.1016/j.bcp.2007.07.019},
   Key = {fds275696}
}

@article{fds275694,
   Author = {Levin, ED and Lawrence, SS and Petro, A and Horton, K and Rezvani, AH and Seidler, FJ and Slotkin, TA},
   Title = {Adolescent vs. adult-onset nicotine self-administration in
             male rats: duration of effect and differential nicotinic
             receptor correlates.},
   Journal = {Neurotoxicology and Teratology},
   Volume = {29},
   Number = {4},
   Pages = {458-465},
   Year = {2007},
   Month = {July},
   ISSN = {0892-0362},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17433619},
   Abstract = {Adolescence is the life stage when tobacco addiction
             typically begins. Adolescent neurobehavioral development may
             be altered by nicotine self-administration in a way that
             persistently potentiates addiction. Previously, we showed
             that female adolescent rats self-administer more nicotine
             than do adults and that the increased nicotine intake then
             persists through the transition to adulthood [E.D. Levin, A.
             Rezvani, D. Montoya, J. Rose, H. Swartzwelder,
             Adolescent-onset nicotine self-administration modeled in
             female rats, Psychopharmacology 169 (2003) 141-149.]. In the
             current study, male Sprague-Dawley rats were given access to
             nicotine via the standard operant IV self-administration
             procedure (nicotine bitartrate dose of 0.03 mg/kg/infusion).
             One group of male rats started during adolescence the other
             group started in young adulthood. After the end of the
             four-week period of self-administration brain regions of the
             rats were assessed for alpha4beta2 nicotinic receptor
             binding. We found that male rats, like females, show higher
             nicotine self-administration when starting during
             adolescence as compared to starting in adulthood (p<0.001).
             Indeed, the effect in adolescent males was even greater than
             that in females, with more than triple the rate of nicotine
             self-administration vs. the adult-onset group during the
             first 2 weeks. The adolescent onset nicotine-self-administering
             rats also had significantly greater high affinity nicotinic
             receptor binding in the midbrain and the striatum, whereas
             hippocampal binding did not differ between the age groups.
             Striatal values significantly correlated with nicotine
             self-administration during the first 2 weeks in the
             adult-onset group but not the adolescent-onset rats,
             suggesting that the differences in self-administration may
             depend in part on underlying disparities in synaptic
             responses to nicotine. After the initial 2 weeks, nicotine
             self-administration in male rats declined toward adult-like
             levels, as the adolescent rats approached adulthood. This
             study showed that adolescent male rats self-administer
             significantly more nicotine than do male adult rats, but
             that adolescent-onset nicotine self-administration in male
             rats declines over weeks of continued use to approach
             adult-onset levels. In a previous study, we found that
             female rats also show greater nicotine self-administration
             with adolescent onset vs. adult onset, but that the females
             continued higher rates of self-administration into
             adulthood. Our results thus reinforce the concept that the
             adolescent brain is unusually receptive to the effects of
             nicotine in a manner that reinforces the potential for
             addiction.},
   Doi = {10.1016/j.ntt.2007.02.002},
   Key = {fds275694}
}

@article{fds275669,
   Author = {Rezvani, AH and Overstreet, DH and Cleves, M and Parsian,
             A},
   Title = {Further genetic characterization of the fawn-hooded (FH/Wjd)
             rat, an animal model of comorbid depression and
             alcoholism.},
   Journal = {Psychiatric Genetics},
   Volume = {17},
   Number = {2},
   Pages = {77-83},
   Year = {2007},
   Month = {April},
   ISSN = {0955-8829},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17413446},
   Keywords = {Alcoholism • Animals • Comorbidity •
             Depressive Disorder • Disease Models, Animal •
             Female • Hair Color • Male • Rats •
             Rats, Mutant Strains* • Reward • epidemiology*
             • genetics • genetics*},
   Abstract = {OBJECTIVE: The main objective of this study was a more
             detailed genetic characterization of the alcohol preferring
             fawn-hooded rat and its intercrosses. Fawn-hooded rats drink
             substantially more alcohol voluntarily than the ACI rats.
             The fawn-hooded rats were shown to be more immobile in the
             forced-swimming test and to drink more saccharin. Recent
             comparisons of the parental strains with F1 and F2
             intercrosses revealed that the alcohol and saccharin intakes
             were positively correlated with each other but not with
             immobility. METHODS: The F1 and F2 progeny were generated by
             intercrossing the fawn-hooded and ACI/N rats. Data from the
             F2 progeny, their F1 parents and progenitors were used to
             estimate heritability. RESULTS: Heritability was estimated
             for alcohol intake (75.6% in males and 67.1% in females),
             alcohol preference (64.7% in males and 39.2% in females),
             saccharin intake (50.8% in males and 37.5% in females), and
             immobility (50.2% in males and 72.1% in females). This same
             data provided estimates of the number of genes involved in
             these phenotypes between three and six. We also took
             advantage of the fact that both progenitor strains are
             pigmented, so a tremendous variety of coat colors were
             present in the F2 progeny (i.e. black, black-hooded, agouti,
             agouti-hooded, fawn, fawn-hooded, orange, and
             orange-hooded). Coat color analyses indicated that none of
             the variables significantly varied with coat color. A high
             correlation however, was observed between alcohol intake and
             preference in each group. Significant correlations between
             alcohol and saccharin intakes were seen only in some groups.
             CONCLUSION: These findings suggest that these phenotypes
             might be regulated by multiple genes, which could be
             detected in quantitative trait loci. These analyses are
             currently underway and will provide a novel approach in
             understanding the genetics of voluntary alcohol
             drinking.},
   Language = {eng},
   Doi = {10.1097/YPG.0b013e328012d7c3},
   Key = {fds275669}
}

@article{fds216640,
   Author = {ED Levin and SS Lawrence and A Petro and K Horton and AH Rezvani and FJ
             Seidler, TA Slotkin},
   Title = {Adolescent vs. adult-onset nicotine self-administration in
             male rats: duration of effect and differential nicotinic
             receptor correlates.},
   Journal = {Neurotoxicology and teratology},
   Volume = {29},
   Number = {4},
   Pages = {458-65},
   Year = {2007},
   Month = {March},
   ISSN = {0892-0362},
   url = {http://dx.doi.org/10.1016/j.ntt.2007.02.002},
   Keywords = {Aging • Animals • Behavior, Animal • Brain
             • Male • Nicotine • Nicotinic Agonists •
             Protein Binding • Rats • Receptors, Nicotinic
             • Regression Analysis • Self Administration •
             administration & dosage* • anatomy & histology •
             drug effects • metabolism • metabolism* •
             methods • physiology • physiology*},
   Abstract = {Adolescence is the life stage when tobacco addiction
             typically begins. Adolescent neurobehavioral development may
             be altered by nicotine self-administration in a way that
             persistently potentiates addiction. Previously, we showed
             that female adolescent rats self-administer more nicotine
             than do adults and that the increased nicotine intake then
             persists through the transition to adulthood [E.D. Levin, A.
             Rezvani, D. Montoya, J. Rose, H. Swartzwelder,
             Adolescent-onset nicotine self-administration modeled in
             female rats, Psychopharmacology 169 (2003) 141-149.]. In the
             current study, male Sprague-Dawley rats were given access to
             nicotine via the standard operant IV self-administration
             procedure (nicotine bitartrate dose of 0.03 mg/kg/infusion).
             One group of male rats started during adolescence the other
             group started in young adulthood. After the end of the
             four-week period of self-administration brain regions of the
             rats were assessed for alpha4beta2 nicotinic receptor
             binding. We found that male rats, like females, show higher
             nicotine self-administration when starting during
             adolescence as compared to starting in adulthood (p<0.001).
             Indeed, the effect in adolescent males was even greater than
             that in females, with more than triple the rate of nicotine
             self-administration vs. the adult-onset group during the
             first 2 weeks. The adolescent onset nicotine-self-administering
             rats also had significantly greater high affinity nicotinic
             receptor binding in the midbrain and the striatum, whereas
             hippocampal binding did not differ between the age groups.
             Striatal values significantly correlated with nicotine
             self-administration during the first 2 weeks in the
             adult-onset group but not the adolescent-onset rats,
             suggesting that the differences in self-administration may
             depend in part on underlying disparities in synaptic
             responses to nicotine. After the initial 2 weeks, nicotine
             self-administration in male rats declined toward adult-like
             levels, as the adolescent rats approached adulthood. This
             study showed that adolescent male rats self-administer
             significantly more nicotine than do male adult rats, but
             that adolescent-onset nicotine self-administration in male
             rats declines over weeks of continued use to approach
             adult-onset levels. In a previous study, we found that
             female rats also show greater nicotine self-administration
             with adolescent onset vs. adult onset, but that the females
             continued higher rates of self-administration into
             adulthood. Our results thus reinforce the concept that the
             adolescent brain is unusually receptive to the effects of
             nicotine in a manner that reinforces the potential for
             addiction.},
   Language = {eng},
   Doi = {10.1016/j.ntt.2007.02.002},
   Key = {fds216640}
}

@article{fds275668,
   Author = {Patra, B and Overstreet, DH and Rezvani, AH and Cleves, M and Parsian,
             A},
   Title = {Analysis of alcohol-related phenotypes in F2 progeny derived
             from FH/Wjd and ACI/N rat strains reveals independent
             measures and sex differences.},
   Journal = {Behavioural Brain Research},
   Volume = {177},
   Number = {1},
   Pages = {37-44},
   Year = {2007},
   Month = {February},
   ISSN = {0166-4328},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17161877},
   Keywords = {Alcohol Drinking • Alcoholism • Animals •
             Behavior, Animal • Disease Models, Animal •
             Drinking • Immobility Response, Tonic • Phenotype*
             • Rats • Rats, Inbred Strains • Sex
             Characteristics* • Species Specificity •
             Statistics, Nonparametric • Swimming • genetics
             • genetics* • physiopathology* •
             psychology},
   Abstract = {Ethanol associated addictive behaviors are governed by a
             combination of multiple gene action (polygenic or
             quantitative trait) and environmental factors. We produced
             F2 progeny from F1 crosses derived from the
             alcohol-preferring Fawn-Hooded (FH/Wjd) rat strain and the
             alcohol-nonpreferring ACI/N strain. We compared different
             phenotypes related to alcohol intake in more than 600 F2
             progeny. We found that female rats had significantly higher
             mean voluntary and forced ethanol, water, saccharin and
             total fluid intakes than male rats. Therefore, we compared
             these measures in the top 15th percentile with those in
             bottom 15th percentile of the F2 total ethanol intake
             distribution separately for males and females. The two tail
             comparison of means showed that only the trait of alcohol
             preference differed significantly in both males and females,
             suggesting that alcohol preference is closely related to
             alcohol intake. Because of the detailed information about
             the F1 parents of the F2 progeny, it was possible to
             determine parental effects. For swim test immobility, for
             example, the F2 progeny derived from FA(m)/FA(f) parents
             (ACI maternal inheritance) had the lowest mean value of 130s
             while the F2 progeny from AF/AF parents (FH maternal
             inheritance) had the highest mean value of 157s (p<0.005).
             The F2 progeny derived from FA/AF parents (FH maternal
             inheritance) showed higher mean values of forced alcohol
             intake than FA/FA parents (FH paternal inheritance) (6.58
             and 6.36g/kg/day, respectively) suggesting that the FH
             mother had a significantly (p<0.0001) greater effect on
             forced alcohol intake than the FH father. It is concluded
             from these analyses that alcohol-related phenotypes are
             segregating independently and may be influenced by maternal
             and sex factors.},
   Language = {eng},
   Doi = {10.1016/j.bbr.2006.11.008},
   Key = {fds275668}
}

@article{fds275693,
   Author = {Rezvani, AH and Overstreet, DH and Levin, ED and Rosenthal, DI and Kordik, CP and Reitz, AB and Vaidya, AH},
   Title = {Effects of atypical anxiolytic N-phenyl-2-[1-[3-(2-pyridinylethynyl)benzoyl]-4-piperidine]acetamide
             (JNJ-5234801) on alcohol intake in alcohol-preferring P
             rats.},
   Journal = {Alcoholism, Clinical and Experimental Research},
   Volume = {31},
   Number = {1},
   Pages = {57-63},
   Year = {2007},
   Month = {January},
   ISSN = {0145-6008},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17207102},
   Keywords = {Acute Disease • Alcohol Drinking • Animals •
             Anti-Anxiety Agents • Chronic Disease •
             Dose-Response Relationship, Drug • Drinking • Drug
             Tolerance • Injections, Intraperitoneal • Male
             • Naltrexone • Narcotic Antagonists •
             Piperidines • Pyridines • Rats • drug effects
             • drug therapy* • genetics* • pharmacology
             • pharmacology*},
   Abstract = {BACKGROUND: N-Phenyl-2-[1-[3-(2-pyridinylethynyl)benzoyl]-4-piperidine]acetamide
             (JNJ-5234801) is a structurally novel atypical anxiolytic
             with an overall in vivo profile in animals suggestive of the
             potential to show anxiolytic efficacy in humans at doses
             that will not cause CNS-related side effects. Furthermore,
             unlike the benzodiazepines, JNJ-5234801 does not have an
             adverse interaction with ethanol even at doses 20 to 40
             times the minimal effective dose in the rat elevated plus
             maze (MED=1.0 mg/kg, p.o.). METHODS: In the present study,
             JNJ-5234801 was evaluated for potential efficacy in reducing
             alcohol intake in alcohol-preferring rats.
             Alcohol-preferring P rats were allowed to drink water or
             alcohol (10%, v/v) in a 2-bottle choice procedure. Once
             stable baselines were established, the acute effects of
             JNJ-5234801 [(10-40 mg/kg, intraperitoneally (i.p.)] were
             assessed. In a separate study, chronic treatment with
             JNJ-5234801 (40 mg/kg once daily, i.p.) for 12 consecutive
             days was compared with naltrexone (20 mg/kg, twice daily,
             i.p.). RESULTS: There was a selective dose-dependent
             reduction in alcohol intake in the alcohol-preferring (P)
             rats after acute administration of JNJ-5234801 (10-40 mg/kg,
             i.p.). There were no significant effects on food or water
             intake. When administered subchronically, both JNJ-5234801
             (40 mg/kg once daily, i.p.) and naltrexone (20 mg/kg, twice
             daily, i.p.) considerably reduced alcohol intake, but
             tolerance to the alcohol-suppressing effects appeared to
             occur sooner in the naltrexone-treated group. While both
             compounds slightly but significantly reduced food intake at
             the beginning, only JNJ-5234801 increased water intake and
             decreased alcohol preference. CONCLUSIONS: The novel
             atypical anxiolytic JNJ-5234801 has a favorable profile
             effects on alcohol intake and related measures compared with
             naltrexone, which is recommended for the treatment of
             alcoholism.},
   Language = {eng},
   Doi = {10.1111/j.1530-0277.2006.00264.x},
   Key = {fds275693}
}

@article{fds275667,
   Author = {Overstreet, DH and Rezvani, AH and Djouma, E and Parsian, A and Lawrence, AJ},
   Title = {Depressive-like behavior and high alcohol drinking co-occur
             in the FH/WJD rat but appear to be under independent genetic
             control.},
   Journal = {Neuroscience and Biobehavioral Reviews},
   Volume = {31},
   Number = {1},
   Pages = {103-114},
   Year = {2007},
   ISSN = {0149-7634},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16982094},
   Keywords = {Alcohol Drinking • Alcoholism • Animals •
             Depression • Depressive Disorder • Disease Models,
             Animal • Genetic Predisposition to Disease •
             Genetics, Behavioral • Immobility Response, Tonic
             • Phenotype • Rats • Rats, Inbred Strains
             • complications • genetics* •
             physiology},
   Abstract = {This review will consider the evidence supporting the view
             that a specific substrain of Fawn-Hooded rat (FH/Wjd)
             exhibits co-occurring depressive-like behavior and high
             alcohol intake independently. First, the FH/Wjd rat is
             compared with other Fawn-Hooded substrains (FH/Har, FHH/Eur,
             FHL/Eur) and it is concluded that only the FH/Wjd rat is
             both highly immobile in the forced swim test and drinks
             substantial amounts of 5-10% alcohol voluntarily. Next it is
             demonstrated that the FH/Wjd rat fulfils many of the
             criteria proposed for an animal model of alcoholism (becomes
             tolerant, becomes dependent and expresses withdrawal
             symptoms, bar-presses for alcohol). Other literature in
             addition to the high swim test immobility suggests that the
             FH/Wjd rat may also be an animal model of depression (high
             basal corticosterone levels, blunted hormonal responses to
             serotonergic agonists). To study the phenotypes more closely
             an inbred strain (ACI/N) of rat that drank little alcohol
             voluntarily and exhibited considerable swimming in the
             forced swim test (i.e., low immobility) was obtained. A
             systematic intercrossing of the parental strains and the
             resulting F1 progeny was carried out to generate more than
             800 F2s. Swim test immobility, alcohol intake and preference
             and saccharin intake are four of the 7 variables assessed in
             each of these rats. Using classical quantitative genetics
             methods, it was determined that these four phenotypes
             exhibited modest heritability and were influenced by
             multiple genes. Correlation coefficients between immobility
             and the other measures were near zero, whereas alcohol
             intake and preference were highly correlated (r=0.9) and
             alcohol and saccharin intakes were modestly correlated
             (r=0.3). A final study showed that chronic fluoxetine
             treatment counteracted the high immobility but did not
             affect alcohol intake, similar to human studies. These
             findings suggest that although depressive-like behavior and
             high alcohol intake co-occur in the FH/Wjd rat, they are
             independently regulated.},
   Language = {eng},
   Doi = {10.1016/j.neubiorev.2006.07.002},
   Key = {fds275667}
}

@article{fds275695,
   Author = {Ryan, JC and Dechraoui, M-YB and Morey, JS and Rezvani, A and Levin, ED and Gordon, CJ and Ramsdell, JS and Dolah, FMV},
   Title = {Transcriptional profiling of whole blood and serum protein
             analysis of mice exposed to the neurotoxin Pacific
             Ciguatoxin-1},
   Journal = {Neurotoxicology},
   Volume = {28},
   Number = {6},
   Pages = {1099-1109},
   Year = {2007},
   ISSN = {0161-813X},
   url = {http://dx.doi.org/10.1016/j.neuro.2007.05.013},
   Abstract = {Ciguatoxins (CTX) are a suite of cyclic polyether toxins
             produced by the marine dinoflagellate Gambierdiscus sp., are
             potent activators of voltage-gated sodium channels and a
             leading cause of human poisoning from food fish. This report
             characterizes the genomic and proteomic response in whole
             blood of adult male mice exposed i.p. to 264 ng/kg of the
             Pacific congener of CTX (P-CTX-1) at 1, 4 and 24 h. Whole
             genome microarray expression data were filtered by tightness
             of fit between replicates, fold change (1.8) and p-value
             (10-5), resulting in 183 annotated genes used for trending
             analysis, K-means clustering and ontology classification.
             Genes involved with cytokine signaling, proteasome complex
             and ribosomal function were dominant. qPCR performed on 19
             genes of interest had a correlation of 0.95 to array results
             by Pearson's correlation coefficient. Serum protein analysis
             showed small but significant changes in 6 of 60 proteins
             assayed: Ccl2, Ccl12, CD40, IL-10, leptin and M-CSF. In
             large part, the gene expression was consistent with a Th2
             immune response with interesting similarities to expression
             seen in asthmatic models. © 2007 Elsevier Inc. All rights
             reserved.},
   Doi = {10.1016/j.neuro.2007.05.013},
   Key = {fds275695}
}

@article{fds275666,
   Author = {Overstreet, DH and Rezvani, AH and Cowen, M and Chen, F and Lawrence,
             AJ},
   Title = {Modulation of high alcohol drinking in the inbred
             Fawn-Hooded (FH/Wjd) rat strain: implications for
             treatment.},
   Journal = {Addiction Biology},
   Volume = {11},
   Number = {3-4},
   Pages = {356-373},
   Year = {2006},
   Month = {September},
   ISSN = {1355-6215},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16961764},
   Keywords = {Alcoholism • Animals • Choice Behavior •
             Disease Models, Animal • Excitatory Amino Acid
             Antagonists • Ibogaine • Naltrexone •
             Narcotics • Phytotherapy • Piperazines •
             Point Mutation • Pueraria • Rats • Rats,
             Inbred Strains • Receptors, Opioid • Serotonin
             • Serotonin Antagonists • drug therapy* •
             genetics • pharmacology • physiology •
             physiopathology • therapeutic use • therapeutic
             use*},
   Abstract = {The Fawn-Hooded rat (FH/Wjd) is an inbred alcohol-preferring
             rat strain, unlike most of the other strains that were
             selectively bred for high alcohol intake and preference. It
             was chosen for study some 16 years ago because of a reported
             mutation that disrupted platelet serotonin function.
             Although the FH/Wjd rat has high alcohol intake (>5
             g/kg/day) and preference (>65%), interbreeding with an
             alcohol-non-preferring inbred strain suggested that these
             measures are unrelated to the serotonin abnormality.
             Similarly, the exaggerated immobility of the FH/Wjd rats in
             the forced swim test did not correlate with the high alcohol
             intake. Many compounds have been tested in the FH/Wjd rats
             after both acute and chronic treatment and a substantial
             number of them have proved effective. However, as the case
             with opiate antagonists, tolerance to the effects of the
             drug can develop. An up-regulation of opioid receptors
             accompanied the chronic treatment and this mechanism may
             account for the development of tolerance. Tolerance to
             opiate antagonists has also been demonstrated in two of the
             selectively bred alcohol-preferring rat lines, but it is
             unknown whether this process may contribute to the relapses
             seen in individuals being treated with naltrexone. Other
             drugs that reliably decrease alcohol intake in the FH/Wjd
             rats include the 5-hydroxytryptamine-2A receptor antagonist,
             amperozide, the mGlu5 receptor antagonist
             3-[(2-methyl-1,3-thiazol-4-yl)ethynyl]pyridine (MTEP) and
             herbal derivatives such as ibogaine, St. John's wort and
             kudzu extract. Thus, studies in the FH/Wjd rat have led to
             the discovery of a wide variety of targets for the
             development of novel agents to treat alcoholism. The fact
             that several of these drugs were shown to reduce alcohol
             intake in some of the selectively bred alcohol-preferring
             rat lines and/or alcohol-preferring vervet monkeys increases
             our confidence that they are good candidates for further
             development.},
   Language = {eng},
   Doi = {10.1111/j.1369-1600.2006.00033.x},
   Key = {fds275666}
}

@article{fds216613,
   Author = {AH Rezvani and DP Caldwell and ED Levin},
   Title = {Chronic nicotine interactions with clozapine and risperidone
             and attentional function in rats.},
   Journal = {Progress in neuro-psychopharmacology & biological
             psychiatry},
   Volume = {30},
   Number = {2},
   Pages = {190-7},
   Year = {2006},
   Month = {March},
   ISSN = {0278-5846},
   url = {http://dx.doi.org/10.1016/j.pnpbp.2005.10.017},
   Keywords = {Animals • Antipsychotic Agents • Attention •
             Behavior, Animal • Clozapine • Conditioning,
             Operant • Dose-Response Relationship, Drug • Drug
             Administration Schedule • Drug Interactions •
             Female • Nicotine • Nicotinic Agonists • Rats
             • Rats, Sprague-Dawley • Reaction Time •
             Risperidone • Sensory Thresholds • Signal
             Detection, Psychological • administration & dosage*
             • drug effects • drug effects* •
             pharmacology*},
   Abstract = {Although antipsychotic drugs are therapeutically effective
             in attenuating the hallmark symptoms of schizophrenia, these
             improvements do not return most patients to normative
             standards of cognitive function. Thus, complementary drug
             treatment may be needed to treat the attentional deficits of
             schizophrenia as well as to counteract the potential
             attentional impairments caused by some antipsychotic drugs.
             Nicotine, a drug commonly self-administered by a great
             majority of individuals with schizophrenia, has been shown
             to significantly improve cognitive function in some studies.
             The current study was conducted to determine the interactive
             effects of the atypical antipsychotic drugs clozapine and
             risperidone with chronic nicotine administration on
             attentional performance. Adult female Sprague-Dawley rats
             (N=35) were trained to perform an attentional task using an
             operant visual signal detection task. After training, rats
             were infused with a dose of 5 mg/kg/day (s.c.) nicotine base
             (n=18) or saline (n=17) for 28 consecutive days via osmotic
             pump. In Exp. 1, while being administered chronic nicotine
             or saline, rats were given acute doses of clozapine (0,
             0.625, 1.25 and 2.5 mg/kg, s.c.) and were tested for
             attentional function. In Exp. 2, while on chronic nicotine
             or saline, other rats were challenged with acute doses of
             risperidone (0, 0.025, 0.05 and 0.1 mg/kg, s.c.) and were
             tested for attentional function. Results showed that acute
             administration of clozapine caused a significant
             dose-dependent impairment in choice accuracy (percent hit)
             in animals treated with chronic saline. Chronic nicotine
             treatment itself lowered accuracy, but attenuated further
             declines with acute clozapine treatment. Acute
             administration of risperidone at high dose significantly
             reduced performance (percent correct rejection) in
             chronically saline-treated rats, but in a similar fashion as
             in Exp. 1, chronic nicotine lowered accuracy but attenuated
             further impairment with acute risperidone. In summary,
             atypical antipsychotic drugs clozapine and risperidone
             significantly impaired choice accuracy in the visual signal
             detection task. Clozapine was more detrimental than
             risperidone but the adverse effects of both clozapine and
             risperidone on attentional performance were masked in rats
             chronically treated with nicotine.},
   Language = {eng},
   Doi = {10.1016/j.pnpbp.2005.10.017},
   Key = {fds216613}
}

@article{fds275691,
   Author = {Levin, ED and McClernon, FJ and Rezvani, AH},
   Title = {Nicotinic effects on cognitive function: behavioral
             characterization, pharmacological specification, and
             anatomic localization.},
   Journal = {Psychopharmacology},
   Volume = {184},
   Number = {3-4},
   Pages = {523-539},
   Year = {2006},
   Month = {March},
   ISSN = {0033-3158},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16220335},
   Keywords = {Alzheimer Disease • Amygdala • Animals •
             Attention • Cognition • Hippocampus • Humans
             • Learning • Memory • Mice • Nicotine
             • Rats • Receptors, Nicotinic • Schizophrenia
             • drug effects • drug effects* • drug therapy
             • pharmacology*},
   Abstract = {Nicotine has been shown in a variety of studies in humans
             and experimental animals to improve cognitive function.
             Nicotinic treatments are being developed as therapeutic
             treatments for cognitive dysfunction.Critical for the
             development of nicotinic therapeutics is an understanding of
             the neurobehavioral bases for nicotinic involvement in
             cognitive function.Specific and diverse cognitive functions
             affected by nicotinic treatments are reviewed, including
             attention, learning, and memory. The neural substrates for
             these behavioral actions involve the identification of the
             critical pharmacologic receptor targets, in particular brain
             locations, and how those incipient targets integrate with
             broader neural systems involved with cognitive
             function.Nicotine and nicotinic agonists can improve working
             memory function, learning, and attention. Both alpha4beta2
             and alpha7 nicotinic receptors appear to be critical for
             memory function. The hippocampus and the amygdala in
             particular have been found to be important for memory, with
             decreased nicotinic activity in these areas impairing
             memory. Nicotine and nicotinic analogs have shown promise
             for inducing cognitive improvement. Positive therapeutic
             effects have been seen in initial studies with a variety of
             cognitive dysfunctions, including Alzheimer's disease,
             age-associated memory impairment, schizophrenia, and
             attention deficit hyperactivity disorder.Discovery of the
             behavioral, pharmacological, and anatomic specificity of
             nicotinic effects on learning, memory, and attention not
             only aids the understanding of nicotinic involvement in the
             basis of cognitive function, but also helps in the
             development of novel nicotinic treatments for cognitive
             dysfunction. Nicotinic treatments directed at specific
             receptor subtypes and nicotinic cotreatments with drugs
             affecting interacting transmitter systems may provide
             cognitive benefits most relevant to different syndromes of
             cognitive impairment such as Alzheimer's disease,
             schizophrenia, and attention deficit hyperactivity disorder.
             Further research is necessary in order to determine the
             efficacy and safety of nicotinic treatments of these
             cognitive disorders.},
   Language = {eng},
   Doi = {10.1007/s00213-005-0164-7},
   Key = {fds275691}
}

@article{fds275692,
   Author = {Rezvani, AH and Caldwell, DP and Levin, ED},
   Title = {Chronic nicotine interactions with clozapine and risperidone
             and attentional function in rats.},
   Journal = {Progress in Neuro Psychopharmacology & Biological
             Psychiatry},
   Volume = {30},
   Number = {2},
   Pages = {190-197},
   Year = {2006},
   Month = {March},
   ISSN = {0278-5846},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16310917},
   Keywords = {Animals • Antipsychotic Agents • Attention •
             Behavior, Animal • Clozapine • Conditioning,
             Operant • Dose-Response Relationship, Drug • Drug
             Administration Schedule • Drug Interactions •
             Female • Nicotine • Nicotinic Agonists • Rats
             • Rats, Sprague-Dawley • Reaction Time •
             Risperidone • Sensory Thresholds • Signal
             Detection, Psychological • administration & dosage*
             • drug effects • drug effects* •
             pharmacology*},
   Abstract = {Although antipsychotic drugs are therapeutically effective
             in attenuating the hallmark symptoms of schizophrenia, these
             improvements do not return most patients to normative
             standards of cognitive function. Thus, complementary drug
             treatment may be needed to treat the attentional deficits of
             schizophrenia as well as to counteract the potential
             attentional impairments caused by some antipsychotic drugs.
             Nicotine, a drug commonly self-administered by a great
             majority of individuals with schizophrenia, has been shown
             to significantly improve cognitive function in some studies.
             The current study was conducted to determine the interactive
             effects of the atypical antipsychotic drugs clozapine and
             risperidone with chronic nicotine administration on
             attentional performance. Adult female Sprague-Dawley rats
             (N=35) were trained to perform an attentional task using an
             operant visual signal detection task. After training, rats
             were infused with a dose of 5 mg/kg/day (s.c.) nicotine base
             (n=18) or saline (n=17) for 28 consecutive days via osmotic
             pump. In Exp. 1, while being administered chronic nicotine
             or saline, rats were given acute doses of clozapine (0,
             0.625, 1.25 and 2.5 mg/kg, s.c.) and were tested for
             attentional function. In Exp. 2, while on chronic nicotine
             or saline, other rats were challenged with acute doses of
             risperidone (0, 0.025, 0.05 and 0.1 mg/kg, s.c.) and were
             tested for attentional function. Results showed that acute
             administration of clozapine caused a significant
             dose-dependent impairment in choice accuracy (percent hit)
             in animals treated with chronic saline. Chronic nicotine
             treatment itself lowered accuracy, but attenuated further
             declines with acute clozapine treatment. Acute
             administration of risperidone at high dose significantly
             reduced performance (percent correct rejection) in
             chronically saline-treated rats, but in a similar fashion as
             in Exp. 1, chronic nicotine lowered accuracy but attenuated
             further impairment with acute risperidone. In summary,
             atypical antipsychotic drugs clozapine and risperidone
             significantly impaired choice accuracy in the visual signal
             detection task. Clozapine was more detrimental than
             risperidone but the adverse effects of both clozapine and
             risperidone on attentional performance were masked in rats
             chronically treated with nicotine.},
   Language = {eng},
   Doi = {10.1016/j.pnpbp.2005.10.017},
   Key = {fds275692}
}

@article{fds275690,
   Author = {Levin, ED and Rezvani, AH},
   Title = {Nicotinic-antipsychotic drug interactions and cognitive
             function.},
   Journal = {Exs},
   Volume = {98},
   Pages = {185-205},
   Year = {2006},
   ISSN = {1023-294X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17019889},
   Keywords = {Animals • Antipsychotic Agents • Cognition •
             Drug Interactions • Humans • Nicotine •
             Schizophrenia • drug effects* • drug therapy
             • metabolism • metabolism* • pharmacology*
             • physiology},
   Abstract = {In summary, neuronal nicotinic systems are important for a
             variety of aspects of cognitive function impacted by
             antipsychotic drugs. It has been demonstrated that
             antipsychotic drugs have memory and attentional impairing
             effects when given to unimpaired subjects. Nicotine can
             reduce some of these impairments, but antipsychotic drug
             administration can also attenuate nicotine effects. We have
             found that nicotinic agonists selective for alpha7 and
             alpha4beta2 receptor subtypes significantly improve learning
             and memory. Serotonergic actions of antipsychotic drugs may
             decrease efficacy of nicotinic co-treatments. When the
             antipsychotic drug clozapine and nicotine are administered
             to subjects with cognitive impairments caused by NMDA
             glutamate receptor blockade or hippocampal dysfunction they
             can significantly attenuate the attentional and memory
             impairments. Nicotine has been shown in our studies to
             reverse the memory impairment caused by acute
             clozapine-induced memory improvement. Acute risperidone and
             haloperidol has been shown to attenuate nicotine-induced
             memory improvement. We have determined the role of
             hippocampal alpha7 and alpha4beta2 nicotinic receptors in
             the neural basis of nicotinic antipsychotic interactions.
             Local acute and chronic hippocampal infusion of either
             nicotinic alpha7 or alpha4beta2 antagonists cause
             significant spatial working memory impairment. Chronic
             hippocampal nicotinic antagonist infusions have served as a
             model of persistent decreases in nicotinic receptor level
             seen in schizophrenia and Alzheimer's disease. Clozapine
             attenuated the memory deficit caused by chronic suppression
             of hippocampal alpha4beta2 receptors while the amnestic
             effects of clozapine were potentiated by chronic suppression
             of hippocampal alpha7 receptors. Nicotinic co-treatment may
             be a useful adjunct in the treatment of schizophrenia, to
             attenuate cognitive impairment of schizophrenia. Nicotine as
             well as selective nicotinic alpha7 and alpha4beta2 receptor
             agonists significantly improve working memory and
             attentional function. Nicotine treatment was found to be
             effective in attenuating the attentional and memory
             impairments caused by the psychototmimetic NMDA antagonist
             dizocilpine (MK-801), a model of the cognitive impairment of
             schizophrenia. Studies of the interactions of antipsychotic
             drugs with nicotinic agents provided quite useful
             information concerning possible co-treatment of people with
             schizophrenia with nicotinic therapy. Nicotine was found to
             significantly attenuate the memory impairments caused by the
             antipsychotic drugs clozapine and olanzapine. Interestingly,
             nicotine-induced cognitive improvement was significantly
             attenuated by the antipsychotic drug clozapine. One of the
             principal effects of clozapine is to block 5HT2 receptors.
             Ketanserin a 5HT2 antagonist significantly attenuated
             nicotine-induced improvements in attention and memory. Thus
             it appears that antipsychotic drugs with actions blocking
             5HT2 receptors may limit the efficacy of nicotinic
             co-treatments for cognitive enhancement.},
   Language = {eng},
   Key = {fds275690}
}

@article{fds275689,
   Author = {Barron, S and White, A and Swartzwelder, HS and Bell, RL and Rodd, ZA and Slawecki, CJ and Ehlers, CL and Levin, ED and Rezvani, AH and Spear,
             LP},
   Title = {Adolescent vulnerabilities to chronic alcohol or nicotine
             exposure: findings from rodent models.},
   Journal = {Alcoholism, Clinical and Experimental Research},
   Volume = {29},
   Number = {9},
   Pages = {1720-1725},
   Year = {2005},
   Month = {September},
   ISSN = {0145-6008},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16205372},
   Keywords = {Adolescent • Adult • Age Factors • Alcoholism
             • Animals • Brain • Cognition • Ethanol
             • Humans • Models, Animal • Nicotine •
             Rats • Smoking • adverse effects •
             complications • drug effects • drug effects*
             • physiology • toxicity*},
   Abstract = {This article presents an overview of the proceedings from a
             symposium entitled "Is adolescence special? Possible
             age-related vulnerabilities to chronic alcohol or nicotine
             exposure," organized by Susan Barron and Linda Spear and
             held at the 2004 Research Society on Alcoholism Meeting in
             Vancouver, British Columbia. This symposium, co-sponsored by
             the Fetal Alcohol Syndrome Study Group and the
             Neurobehavioral Teratology Society, focused on our current
             knowledge regarding the long-term consequences of ethanol
             and/or nicotine exposure during adolescence with the
             emphasis on data from rodent models. The support from these
             two societies represents the understanding by these research
             groups that adolescence represents a unique developmental
             stage for the effects of chronic drug exposure and also
             marks an age in which many risky behaviors including alcohol
             consumption and smoking typically begin. The speakers
             included (1) Aaron White, who presented data on the effects
             of adolescent ethanol exposure on subsequent motor or
             cognitive response to an ethanol challenge in adulthood; (2)
             Richard Bell, who presented data suggesting that genetic
             differences could play a role in adolescent vulnerability to
             ethanol; (3) Craig Slawecki, who presented data looking at
             the effects of chronic exposure to alcohol or nicotine on
             neurophysiologic and behavioral end points; and (4) Ed
             Levin, who presented data on acute and long-term
             consequences of adolescent nicotine exposure. Finally, Linda
             Spear provided some summary points and recommendations
             regarding unresolved issues and future directions.},
   Language = {eng},
   Doi = {10.1097/01.alc.0000179220.79356.e5},
   Key = {fds275689}
}

@article{fds275688,
   Author = {Rezvani, AH and Caldwell, DP and Levin, ED},
   Title = {Nicotinic-serotonergic drug interactions and attentional
             performance in rats.},
   Journal = {Psychopharmacology},
   Volume = {179},
   Number = {3},
   Pages = {521-528},
   Year = {2005},
   Month = {May},
   ISSN = {0033-3158},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15682310},
   Keywords = {Animals • Attention • Dose-Response Relationship,
             Drug • Drug Interactions • Female •
             Ketanserin • Nicotine • Psychomotor Performance
             • Rats • Rats, Sprague-Dawley • Receptor,
             Serotonin, 5-HT2A • Serotonin 5-HT2 Receptor
             Antagonists • Serotonin Antagonists • drug
             effects* • pharmacology • pharmacology* •
             physiology},
   Abstract = {RATIONALE: Both central serotonergic and nicotinic systems
             play important roles in a variety of neurobehavioral
             functions; however, the interactions of these two systems
             have not been fully characterized. The current study served
             to determine the impact of a relatively selective 5-HT2A
             receptor antagonist, ketanserin, on attentional function in
             rats and the interactions of ketanserin with nicotine
             administration. METHODS: A standard operant visual signal
             detection task was used to assess sustained attention. In
             expt 1, adult female Sprague-Dawley rats (n = 39) were
             injected subcutaneously (SC) with a dose range of ketanserin
             (0, 0.25, 0.5 and 1 mg/kg). In expt 2, the interactions of
             acute ketanserin (0, 1 and 2 mg/kg, SC) and acute nicotine
             (0, 25 and 50 microg/kg, SC) were assessed. In expt 3, the
             interaction of acute ketanserin (0, 1 and 2 mg/kg, SC) and
             chronic nicotine (5 mg/kg per day, SC for 4 weeks via
             osmotic pump) was characterized. Using an operant visual
             signal detection task, three possible outcomes (dependent
             variables) were measured in each trial: percent hit, percent
             correct rejection, and response omissions. RESULTS:
             Ketanserin, when given alone, did not have a significant
             effect on either percent hit or percent correct rejection.
             Acute administration of 25 microg/kg nicotine significantly
             improved percent hit (i.e. improvement in choice accuracy),
             an effect that was reversed by acute administration of 1
             mg/kg ketanserin. Chronic nicotine infusion for 28
             consecutive days significantly increased percent correct
             rejection (i.e. improvement in choice accuracy) without
             development of tolerance, an effect which was reversed by an
             acute dose of 2 mg/kg ketanserin. CONCLUSIONS: These data
             suggest a functional interaction between nicotine and 5-HT2A
             receptor antagonist ketanserin.},
   Language = {eng},
   Doi = {10.1007/s00213-004-2060-y},
   Key = {fds275688}
}

@article{fds275687,
   Author = {Levin, ED and Tizabi, Y and Rezvani, AH and Caldwell, DP and Petro, A and Getachew, B},
   Title = {Chronic nicotine and dizocilpine effects on regionally
             specific nicotinic and NMDA glutamate receptor
             binding.},
   Journal = {Brain Research},
   Volume = {1041},
   Number = {2},
   Pages = {132-142},
   Year = {2005},
   Month = {April},
   ISSN = {0006-8993},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15829222},
   Keywords = {Allosteric Regulation • Animals • Binding Sites
             • Binding, Competitive • Brain •
             Bungarotoxins • Cystine • Dizocilpine Maleate
             • Drug Administration Schedule • Drug Interactions
             • Drug Synergism • Excitatory Amino Acid
             Antagonists • Female • Neural Inhibition •
             Nicotine • Nicotinic Agonists • Protein Subunits
             • Rats • Rats, Sprague-Dawley • Receptors,
             N-Methyl-D-Aspartate • Receptors, Nicotinic •
             Startle Reaction • drug effects • drug effects*
             • metabolism • pharmacology • pharmacology*
             • physiology},
   Abstract = {Chronic nicotine administration has long been known to
             increase the number of high-affinity alpha4beta2 nicotinic
             receptors with lesser effects on low-affinity alpha7
             nicotinic receptors. Nicotine has been shown to promote the
             release of a variety of neurotransmitters including
             glutamate. Nicotine may also interact directly with the
             glutamatergic receptors. Nicotinic-glutamate interactions
             may be critical to the long-term effects of nicotine.
             Conversely, glutamatergic drugs may interact with the
             nicotinic system. Such interactions have important
             implications in interpretation of the mechanism of drug
             actions, especially when the drugs are given together. The
             current study examined the effects of chronic administration
             of nicotine (5 mg of the nicotine base/kg/day for 28 days),
             dizocilpine (MK-801) (0.3 mg/kg/day for 28 days), an NMDA
             receptor antagonist, as well as the combination of the two
             drugs on nicotinic and NMDA receptor densities in discrete
             brain regions. The chronic dose of dizocilpine used was
             behaviorally active causing a dramatic reduction in prepulse
             inhibition (PPI) of acoustic startle response. The nicotine
             dose used did not significantly affect PPI but previously we
             have found it to be behaviorally active in improving working
             memory function. High-affinity nicotinic receptor binding,
             as has been seen previously, was significantly increased by
             chronic nicotine in most areas. Chronic dizocilpine alone
             did not affect high-affinity nicotinic receptor binding, but
             it did modify the effects of chronic nicotine, attenuating
             nicotine-induced increases in the frontal cortex and
             striatum. Low-affinity nicotinic binding was significantly
             increased by chronic nicotine in only one area, the
             cerebellum. Chronic dizocilpine significantly increased
             low-affinity nicotinic binding in several brain areas, the
             colliculi, hippocampus, and the hypothalamus. The
             combination of nicotine and dizocilpine attenuated the
             effects of each with diminished nicotine-induced increased
             nicotinic low-affinity binding in the cerebellum and
             diminished dizocilpine-induced increased nicotinic
             low-affinity binding in the hippocampus and hypothalamus. In
             contrast, chronic nicotine and dizocilpine had a mutually
             potentiating effect of increasing nicotinic low-affinity
             binding in the frontal cortex. NMDA receptor binding was
             affected only in the hippocampus, where both dizocilpine and
             nicotine significantly increased binding. Chronic nicotine
             effects on receptor regulation are significantly affected by
             concurrent blockade of NMDA glutamate receptors.},
   Language = {eng},
   Doi = {10.1016/j.brainres.2005.01.104},
   Key = {fds275687}
}

@article{fds275684,
   Author = {Rezvani, AH and Levin, ED},
   Title = {Adolescent and adult rats respond differently to nicotine
             and alcohol: motor activity and body temperature.},
   Journal = {International Journal of Developmental Neuroscience : the
             Official Journal of the International Society for
             Developmental Neuroscience},
   Volume = {22},
   Number = {5-6},
   Pages = {349-354},
   Year = {2004},
   Month = {August},
   ISSN = {0736-5748},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15380834},
   Keywords = {Adaptation, Physiological • Age Factors • Aging
             • Animals • Animals, Newborn • Dose-Response
             Relationship, Drug • Drug Interactions • Ethanol
             • Female • Injections, Intraperitoneal •
             Injections, Subcutaneous • Locomotion • Nicotine
             • Rats • Rats, Sprague-Dawley • Sex Factors
             • administration & dosage* • drug effects •
             drug effects* • physiology • physiology*},
   Abstract = {Alcohol and nicotine are the most widely abused drugs in the
             world. The use of these addictive drugs often begins in
             adolescence, however, little is known about the different
             impacts of nicotine and alcohol on adolescents versus
             adults. This study examined both the individual and combined
             effects of nicotine and alcohol on body temperature and
             locomotor activity in adolescent and adults rats. Rats were
             injected with saline (SC) + saline (IP), nicotine (SC) +
             saline (IP), alcohol (IP) + saline (SC) or alcohol (IP) +
             nicotine (SC). The dose selected for nicotine was 0.2 mg/kg
             and for alcohol 2.5 g/kg (16% v/v). For each age/treatment,
             10-13 animals were used, with each animal receiving only one
             treatment. In regards to body temperature, both nicotine and
             alcohol caused a significant age x drug interaction. The
             combination of nicotine and alcohol caused greater drop in
             body temperature in adolescent than in adult rats. Neither
             of the two drugs, when given alone, caused differential
             effects in adolescents or adult rats, though both resulted
             in drop in body temperature. In terms of locomotor activity,
             the treatment that produced a significantly different effect
             between adolescents and adults was nicotine alone. Nicotine
             significantly decreased locomotor activity in adolescent
             compared to adult rats. These preliminary results suggest
             that adolescent rats may have an increased sensitivity to
             nicotine and alcohol, which may consequently impact their
             initial addiction to these two drugs.},
   Language = {eng},
   Doi = {10.1016/j.ijdevneu.2004.03.007},
   Key = {fds275684}
}

@article{fds275686,
   Author = {Rezvani, AH and Levin, ED},
   Title = {Corrigendum to “Nicotine–antipsychotic drug interactions
             and attentional performance in female rats” [Eur. J.
             Pharmacol. 486 (2004) 175–182]},
   Journal = {European Journal of Pharmacology},
   Volume = {489},
   Number = {3},
   Pages = {215-215},
   Publisher = {Elsevier BV},
   Year = {2004},
   Month = {April},
   url = {http://dx.doi.org/10.1016/j.ejphar.2004.03.009},
   Doi = {10.1016/j.ejphar.2004.03.009},
   Key = {fds275686}
}

@article{fds275685,
   Author = {Rezvani, AH and Levin, ED},
   Title = {Nicotine-antipsychotic drug interactions and attentional
             performance in female rats.},
   Journal = {European Journal of Pharmacology},
   Volume = {486},
   Number = {2},
   Pages = {175-182},
   Year = {2004},
   Month = {February},
   ISSN = {0014-2999},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/14975706},
   Keywords = {Animals • Antipsychotic Agents • Attention •
             Central Nervous System Stimulants • Clozapine •
             Dose-Response Relationship, Drug • Drug Interactions
             • Female • Haloperidol • Nicotine •
             Photic Stimulation • Psychomotor Performance •
             Rats • Rats, Sprague-Dawley • Risperidone •
             administration & dosage • drug effects* •
             pharmacokinetics • pharmacology • pharmacology*
             • physiology},
   Abstract = {Schizophrenia is marked by pronounced cognitive impairments
             in addition to the hallmark psychotic symptoms like
             hallucinations. Antipsychotic drugs can effectively reduce
             these hallucinations; however, the drugs have not resolved
             the cognitive impairment. Interestingly, nicotine, a drug
             commonly self-administered by people with schizophrenia, has
             been shown to significantly improve cognitive function of
             people with schizophrenia. The current study was conducted
             to determine the effect of typical (haloperidol) and
             atypical (clozapine and risperidone) antipsychotic drug
             treatment on sustained attention in rats performing a visual
             signal detection task. In addition, the interaction of
             haloperidol with chronic nicotine administration was
             assessed. Female Sprague-Dawley rats were injected
             subcutaneously with clozapine (0, 0.6, 1.25 and 2.5 mg/kg),
             risperidone (0, 0.025, 0.05 and 0.1 mg/kg) or haloperidol
             (0, 0.01, 0.02 and 0.04 mg/kg). In the second part of the
             study, the interaction of acute haloperidol (0, 0.005, 0.01
             and 0.02 mg/kg) and chronic nicotine (5 mg/kg/day, for 4
             weeks via osmotic minipump) was characterized. Clozapine,
             risperidone and haloperidol all caused dose-related
             impairments in percent hit performance. There was a
             significant linear dose-related impairment in percent hit
             caused by risperidone. All the doses of clozapine caused a
             significant impairment in percent hit at the higher
             luminance intensities in the visual signal detection task.
             The 0.01 and 0.02 mg/kg haloperidol doses caused significant
             decreases in percent hit. The 0.04 mg/kg haloperidol dose
             impaired performance of the task to the point that reliable
             choice accuracy measurements could not be made. Chronic
             nicotine infusion significantly diminished the impairing
             effects of haloperidol on performance during weeks 1-2. In
             summary, both typical and atypical antipsychotic drugs
             significantly impaired sustained attention in rats.
             Haloperidol was more detrimental than clozapine and
             risperidone. Chronic nicotine diminished the adverse effects
             of haloperidol on performance. This study establishes a
             paradigm to reliably determine the attentional impairment
             caused by antipsychotic drugs.},
   Language = {eng},
   Doi = {10.1016/j.ejphar.2003.12.021},
   Key = {fds275685}
}

@article{fds275683,
   Author = {Levin, ED and Rezvani, AH and Montoya, D and Rose, JE and Swartzwelder,
             HS},
   Title = {Adolescent-onset nicotine self-administration modeled in
             female rats.},
   Journal = {Psychopharmacology},
   Volume = {169},
   Number = {2},
   Pages = {141-149},
   Year = {2003},
   Month = {September},
   ISSN = {0033-3158},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12764575},
   Keywords = {Adolescent • Age Factors • Age of Onset* •
             Animals • Disease Models, Animal • Dose-Response
             Relationship, Drug • Female • Humans •
             Hypothermia • Infusions, Intravenous • Injections,
             Subcutaneous • Motor Activity • Nicotine •
             Rats • Rats, Sprague-Dawley • Self Administration*
             • Time Factors • administration & dosage* •
             adverse effects • chemically induced • drug
             effects • pharmacokinetics* • physiology*},
   Abstract = {RATIONALE: Although the great majority of tobacco addiction
             begins during adolescence, little is known about
             differential nicotine effects in adolescents versus adults.
             OBJECTIVES: A rat model was used to determine the impact of
             the age of onset on nicotine self-administration. METHODS:
             In expt 1, nicotine self-administration of female
             Sprague-Dawley rats over a range of acute doses (0.01-0.08
             mg/kg per infusion) was determined in adolescent (beginning
             at 54-62 days) versus adult (beginning at 84-90 days). In
             expt 2, chronic nicotine self-administration over 4 weeks
             from adolescence into adulthood was compared with the
             chronic self-administration beginning in adulthood. In expt
             3, adolescent-adult differences in nicotine effects on body
             temperature and locomotor responses were determined.
             RESULTS: Adolescent-onset rats showed a significant main
             effect of increased nicotine intake compared with
             adult-onset rats in an eight-fold range of acute unit
             doses/infusion. Significant age differences were also seen
             in the chronic level of nicotine self-administration. Over 4
             weeks, the adolescent-onset group had nearly double the rate
             of nicotine self-administration of the benchmark nicotine
             dose (0.03 mg/kg per infusion) compared to the adult-onset
             group. This increased nicotine intake persisted into
             adulthood. Adolescent rats had significantly greater
             response than adults to the hypothermic effects of nicotine,
             but had significantly less response than adults to the
             reduction in locomotor activity seen after nicotine.
             CONCLUSIONS: Adolescent-onset nicotine self-administration
             in female rats was associated with significantly higher
             levels of nicotine self-administration versus rats, which
             began nicotine self-administration in adulthood. This
             greater self-administration persists into adulthood and may
             underlie greater propensity of adolescents to nicotine
             addiction.},
   Language = {eng},
   Doi = {10.1007/s00213-003-1486-y},
   Key = {fds275683}
}

@article{fds275682,
   Author = {Rezvani, AH and Levin, ED},
   Title = {Nicotine-alcohol interactions and attentional performance on
             an operant visual signal detection task in female
             rats.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {76},
   Number = {1},
   Pages = {75-83},
   Year = {2003},
   Month = {August},
   ISSN = {0091-3057},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/13679219},
   Keywords = {Animals • Attention • Conditioning, Operant •
             Dose-Response Relationship, Drug • Drug Interactions
             • Ethanol • Female • Nicotine • Photic
             Stimulation • Psychomotor Performance • Rats
             • Rats, Sprague-Dawley • antagonists & inhibitors
             • drug effects* • methods • pharmacology*
             • physiology},
   Abstract = {Nicotine and alcohol are very often co-used and co-abused.
             Thus, it is important to understand their interactions. In
             many ways, nicotine and alcohol have opposing effects. This
             can be clearly seen in terms of their effects on cognitive
             function. Nicotine effectively improves attention while
             alcohol impairs it. The current study was conducted to
             determine in a rat model the interaction of nicotine and
             alcohol on attention using an operant visual signal
             detection task. It is hypothesized that nicotine would
             reverse the alcohol-induced impairment in accuracy of
             performance in this task. Female Sprague-Dawley rats (N=35)
             were trained on a visual operant signal detection task for
             food reinforcement with 300 trials/session in three equal
             time blocks. The rats were divided into poor and good
             performers according to their predrug baseline performance
             accuracy. The first experiment examined the dose-effect
             function of alcohol (0, 0.375, and 0.75 g/kg i.p.) on this
             task. The lower alcohol dose significantly impaired percent
             correct rejection in the high-performing rats but not the
             low-performing rats. The higher alcohol dose significantly
             impaired percent hit performance during the first two thirds
             of the session in both high- and low-performing groups. The
             second experiment examined alcohol (0.75 g/kg i.p.)
             interactions with nicotine (0, 12.5, 25, and 50 microg/kg
             s.c.) on attentional performance. The 25 and 50 microg/kg
             nicotine doses caused a significant (P<.05) improvement in
             hit accuracy. Alcohol blocked this nicotine-induced
             improvement, even though at this later time it no longer had
             an effect of its own. In the high baseline group, the 25
             microg/kg nicotine dose also caused a significant (P<.025)
             improvement in hit accuracy. As in Experiment 1, the high
             baseline group was not significantly impaired by 0.75 g/kg
             of alcohol. However, this alcohol dose did eliminate the
             nicotine-induced improvement. These results suggest that
             alcohol, when given alone, impairs sustained attention and
             blocks nicotine-induced attentional improvements even when
             it does not cause impairments on its own.},
   Language = {eng},
   Doi = {10.1016/s0091-3057(03)00193-x},
   Key = {fds275682}
}

@article{fds275664,
   Author = {Rezvani, AH and Overstreet, DH and Perfumi, M and Massi,
             M},
   Title = {Plant derivatives in the treatment of alcohol
             dependency.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {75},
   Number = {3},
   Pages = {593-606},
   Year = {2003},
   Month = {June},
   ISSN = {0091-3057},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12895677},
   Keywords = {Alcoholism • Animals • Humans • Hypericum
             • Ibogaine • Plant Extracts • Plants,
             Medicinal* • Pueraria • drug therapy* •
             therapeutic use*},
   Abstract = {The present review summarizes the findings of the effects of
             extracts of purified compounds from several plants on
             alcohol intake in alcohol-preferring rats. These include St.
             John's wort (Hypericum perforatum, HPE), kudzu (Pueraria
             lobata) and ibogaine (Tabernanthe iboga). Alcohol-preferring
             (P), Marchigian Sardinian (msP), high-alcohol-drinking
             (HAD), Fawn-Hooded (FH) rats were allowed to drink alcohol
             or water voluntarily to establish baseline levels. Pure
             compounds (puerarin, daidzin, daidzein or analogs) isolated
             from kudzu, extracts from HPE or ibogaine and its analog
             were given by either intraperitoneal or oral administration.
             After acute administration, all agents dose-dependently
             reduced alcohol intake with minimal effects on food intake.
             Puerarin and HPE were also effective following chronic
             treatment. Overall, it is clear that pure compounds
             (daidzin, puerarin), extracts from St. John's wort, ibogaine
             and an ibogaine analog suppress alcohol intake in animal
             models of excessive drinking with minimal effects on other
             appetitive behaviors. Although the true mechanisms of action
             of these compounds on alcohol intake are not fully
             understood, with the current information, it appears that
             these compounds exert their effects by modulating several
             neuronal systems implicated in drinking behavior. However,
             their role in the future of pharmacotherapy for alcoholism
             will depend upon the outcome of carefully conducted clinical
             trials.},
   Language = {eng},
   Key = {fds275664}
}

@article{fds275681,
   Author = {Rezvani, AH and Levin, ED},
   Title = {Nicotinic-glutamatergic interactions and attentional
             performance on an operant visual signal detection task in
             female rats.},
   Journal = {European Journal of Pharmacology},
   Volume = {465},
   Number = {1-2},
   Pages = {83-90},
   Year = {2003},
   Month = {March},
   ISSN = {0014-2999},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12650836},
   Keywords = {Animals • Attention • Behavior, Animal •
             Conditioning, Operant • Dizocilpine Maleate •
             Dose-Response Relationship, Drug • Drug Interactions
             • Excitatory Amino Acid Antagonists • Male •
             Nicotine • Nicotinic Agonists • Psychomotor
             Performance • Rats • Rats, Sprague-Dawley •
             Signal Detection, Psychological • drug effects •
             drug effects* • pharmacology*},
   Abstract = {Nicotinic systems have been shown to be critically involved
             in cognitive function including attention. Nicotine has been
             shown to improve performance on attentional tasks in humans
             with Alzheimer's disease, schizophrenia and attention
             deficit hyperactivity disorder. Nicotine has mixed effects
             on attentional accuracy in unimpaired rats with findings of
             increased, reduced or unaltered accuracy under different
             conditions. Nicotine effects on attentional function in rats
             might be more clearly seen in reversing impaired
             performance. The current study determined nicotine effects
             on attentional accuracy reduced by the NMDA receptor
             antagonist dizocilpine (MK-801). Sprague-Dawley rats (N=35)
             were trained on a food-motivated two-lever operant task with
             one lever correct after a brief visual signal (0.027-1.22
             lx) for hits and the other lever correct after the absence
             of a signal for correct rejections. First, a dose response
             study of dizocilpine was conducted to determine the
             threshold for impairment. The rats were administered acute
             doses of dizocilpine (0, 12.5, 25 and 50 microg/kg, sc). The
             50 microg/kg dose caused significant (p<0.0005) reduction in
             percent hit at the four highest signal intensities. Percent
             correct rejection was also significantly lowered by this
             dose (p<0.005). No effect was seen with 12.5 microg/kg and
             only minimal effect seen with 25 microg/kg. Then,
             nicotine-dizocilpine interactions were investigated. The
             rats were administered acute doses of dizocilpine (0, 37.5
             and 50 microg/kg, sc) and nicotine (0, 25 and 50 microg/kg,
             sc), alone or in combination. Percent hit was affected by
             nicotine and dizocilpine in a complex fashion with only the
             nicotinexdizocilpinexsignal intensity interaction being
             significant (p<0.05). Percent correct rejection showed a
             more straightforward effect. Percent correct rejection was
             significantly reduced by 50 microg/kg dizocilpine (p<0.025).
             The addition of 25 microg/kg of nicotine significantly
             (p<0.025) reversed the dizocilpine-induced reduction of
             correct rejection. This study shows that dizocilpine reduces
             signal detection accuracy in a dose-dependent fashion.
             Nicotine can partially counteract an aspect of this
             reduction by reversing the dizocilpine-induced reduction of
             correct rejection.},
   Language = {eng},
   Key = {fds275681}
}

@article{fds275663,
   Author = {Chen, F and Rezvani, AH and Lawrence, AJ},
   Title = {Autoradiographic quantification of neurochemical markers of
             serotonin, dopamine and opioid systems in rat brain
             mesolimbic regions following chronic St John's wort
             treatment.},
   Journal = {Naunyn Schmiedeberg'S Archives of Pharmacology},
   Volume = {367},
   Number = {2},
   Pages = {126-133},
   Year = {2003},
   Month = {February},
   ISSN = {0028-1298},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12595953},
   Keywords = {Animals • Antidepressive Agents • Autoradiography
             • Biological Markers • Carrier Proteins •
             Dopamine • Dopamine Plasma Membrane Transport Proteins
             • Hypericum • Limbic System • Male •
             Membrane Glycoproteins • Membrane Transport Proteins
             • Nerve Tissue Proteins* • Opioid Peptides •
             Plant Extracts • Radioligand Assay • Rats •
             Receptor, Serotonin, 5-HT1A • Receptor, Serotonin,
             5-HT2A • Receptors, Opioid, mu • Serotonin •
             Serotonin Plasma Membrane Transport Proteins •
             administration & dosage • analysis • chemistry*
             • drug effects • drug effects* • metabolism
             • metabolism* • pharmacology},
   Abstract = {Effects of chronic treatment with St John's wort (SJW,
             Hypericum perforatum) on neurochemical markers of serotonin,
             dopamine and opioid systems in mesolimbic regions of the
             fawn-hooded rat were investigated by quantitative
             autoradiography. After 10 days' treatment, SJW significantly
             increased [(3)H]citalopram binding to 5-HT transporters in
             multiple mesolimbic regions. In contrast, SJW resulted in a
             region-specific alteration of [(3)H]mazindol binding to
             dopamine transporters, such as increased binding of
             [(3)H]mazindol in the olfactory tubercle and decreased
             binding in the ventral tegmental area. In addition, SJW also
             resulted in differential modulation of the binding
             properties of 5-HT(1A)-, 5-HT(2A)- and mu-opioid receptors
             in a region-specific manner. The ability of SJW to affect
             5-HT, dopamine and opioid systems in mesolimbic regions in
             the CNS, either by a direct or by indirect (adaptation)
             mechanism, may help to explain the efficacy of SJW in the
             treatment of depression clinically and in some of the
             behavioural effects observed in experimental
             rodents.},
   Language = {eng},
   Doi = {10.1007/s00210-002-0666-3},
   Key = {fds275663}
}

@article{fds275665,
   Author = {Overstreet, DH and Keung, W-M and Rezvani, AH and Massi, M and Lee,
             DYW},
   Title = {Herbal remedies for alcoholism: promises and possible
             pitfalls.},
   Journal = {Alcoholism, Clinical and Experimental Research},
   Volume = {27},
   Number = {2},
   Pages = {177-185},
   Year = {2003},
   Month = {February},
   ISSN = {0145-6008},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12605067},
   Keywords = {Alcohol Drinking • Alcoholism • Animals •
             Humans • Hypericum* • Phytotherapy* • Plant
             Extracts • Pueraria* • Rats • prevention &
             control • rehabilitation* • therapeutic
             use*},
   Abstract = {This review summarizes the findings of the effects on
             alcohol intake in alcohol-preferring rats of extracts or
             purified compounds from two of the most promising herbs:
             kudzu (Pueraria lobata) and St. John's Wort (Hypericum
             perforatum). It is a summary of a symposium presented at the
             2002 RSA meeting in San Francisco. The meeting
             organizers/co-chairs were David Overstreet and Wing-Ming
             Keung. The presentations were (1) Introduction to the
             symposium, by David Y. W. Lee and David H. Overstreet; (2)
             Effects of daidzin on alcohol intake-search for mechanisms
             of action, by Wing-Ming Keung; (3) Long-term suppressive
             effects of puerarin on alcohol drinking in rats, by David
             Overstreet and David Y. W. Lee; (4) St. John's Wort extract
             reduces alcohol intake in FH and P rats, by Amir Rezvani and
             David Overstreet; and (5) extracts reduce alcohol intake in
             Marchigian Sardinian alcohol-preferring rats, by Maurizio
             Massi.},
   Language = {eng},
   Doi = {10.1097/01.ALC.0000051022.26489.CF},
   Key = {fds275665}
}

@article{fds275679,
   Author = {Rezvani, AH and Bushnell, PJ and Levin, ED},
   Title = {Effects of nicotine and mecamylamine on choice accuracy in
             an operant visual signal detection task in female
             rats.},
   Journal = {Psychopharmacology},
   Volume = {164},
   Number = {4},
   Pages = {369-375},
   Year = {2002},
   Month = {December},
   ISSN = {0033-3158},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12457266},
   Keywords = {Animals • Attention • Choice Behavior •
             Conditioning, Operant • Contrast Sensitivity •
             Dose-Response Relationship, Drug • Female •
             Mecamylamine • Nicotine • Nicotinic Antagonists
             • Rats • Rats, Sprague-Dawley • Reaction Time
             • Signal Detection, Psychological • drug effects
             • drug effects* • pharmacology*},
   Abstract = {RATIONALE: During the past decade, central nicotinic systems
             have been shown in both experimental animals and humans to
             play an important role in cognitive function. However, the
             way in which specific aspects of cognitive function are
             affected by nicotinic systems has remained unclear. In
             humans, the most pronounced action of nicotine is to improve
             attention, but in rats, memory improvement is more easily
             seen. This may be due to differences in methods for
             assessing attention in rats and humans or to species
             differences in the roles of nicotinic systems in cognitive
             function. In the current study, we explored the effects of
             nicotine and mecamylamine using an operant visual signal
             detection task designed to model sustained attention
             processes common to rats and humans. METHODS: Adult female
             rats ( n=35) were trained to perform the signal detection
             task to a stable baseline of about 75% accuracy. The rats
             were then assigned to two subgroups of high and low accuracy
             based on overall accuracy (hits and correct rejections) at
             the end of training. All rats were then injected (SC, 10 min
             before testing) with saline or different doses of nicotine
             (0.0125, 0.025, 0.05, 0.1, 0.2 and 0.4 mg/kg) or the
             nicotinic antagonist mecamylamine (1, 2 and 4 mg/kg).
             RESULTS: A low dose range of nicotine (0.0125, 0.025, and
             0.05 mg/kg) caused a dose-related increase in percent
             correct rejection. This dose range did not affect correct
             detections of the signal (percent hit). Higher doses of
             nicotine (0.1, 0.2 and 0.4 mg/kg) did not affect percent
             correct rejection, but did have a time-dependent effect on
             percent hit. Early in the session, the higher doses of
             nicotine reduced percent hit, whereas during the later part
             of the session higher doses of nicotine increased percent
             hit. Effects of nicotine did not differ between the high-
             and low-accuracy rats. Mecamylamine decreased choice
             accuracy, reducing both percent hit and percent correct
             rejection. Mecamylamine reduced percent hit in the
             low-accuracy rats at a lower drug dose than in the
             high-accuracy rats. CONCLUSIONS: These results support the
             involvement of nicotinic systems in attention in rats, as
             has been shown in humans. This rat model of sustained
             attention may provide a good approach to studying neural
             mechanisms underlying the effects of nicotinic cholinergic
             receptors on attention and a means to evaluate the potential
             of novel nicotinic agonists to counteract attentional
             dysfunction.},
   Language = {eng},
   Doi = {10.1007/s00213-002-1221-0},
   Key = {fds275679}
}

@article{fds275680,
   Author = {Levin, ED and Rezvani, AH},
   Title = {Nicotinic treatment for cognitive dysfunction.},
   Journal = {Current drug targets. CNS and neurological
             disorders},
   Volume = {1},
   Number = {4},
   Pages = {423-431},
   Year = {2002},
   Month = {August},
   ISSN = {1568-007X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12769614},
   Keywords = {Alzheimer Disease • Animals • Attention Deficit
             Disorder with Hyperactivity • Cognition Disorders
             • Humans • Nicotinic Agonists • Nicotinic
             Antagonists • Schizophrenia • drug therapy •
             drug therapy* • psychology • therapeutic
             use*},
   Abstract = {Nicotinic medications may provide beneficial therapeutic
             treatment for cognitive dysfunction such as Alzheimer's
             disease, schizophrenia and attention deficit hyperactivity
             disorder (ADHD). For development of nicotinic treatments we
             are fortunate to have a well characterized lead compound,
             nicotine. Transdermal nicotine patches offer a way to
             deliver measured doses of nicotine in a considerably safer
             fashion than the more traditional means of administration,
             tobacco smoking. We have found that transdermal nicotine
             significantly improves attentional function in people with
             Alzheimer's disease, schizophrenia or ADHD as well as normal
             nonsmoking adults. To follow-up on this proof of principal
             that nicotinic treatment of cognitive dysfunction holds
             promise, it is important to use animal models to determine
             the critical neurobehavioral bases for nicotinic involvement
             in cognitive function so that more selective nicotinic
             analogues that improve cognitive function with fewer side
             effects can be developed. We have found with local infusion
             in rat studies that the hippocampus and amygdala are
             important substrates for nicotinic effects on working memory
             function. Both alpha7 and alpha4beta2 nicotinic receptors
             are involved in working memory. Nicotinic interactions with
             dopaminergic and glutaminergic systems are also important in
             the basis of cognitive function. Studies of the neural
             nicotinic mechanisms underlying cognitive function are key
             for opening avenues for development of safe and effective
             nicotinic treatments for cognitive dysfunction.},
   Language = {eng},
   Key = {fds275680}
}

@article{fds275678,
   Author = {Rezvani, AH and Levin, ED},
   Title = {Nicotine-alcohol interactions and cognitive function in
             rats.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {72},
   Number = {4},
   Pages = {865-872},
   Year = {2002},
   Month = {July},
   ISSN = {0091-3057},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12062576},
   Keywords = {Animals • Body Temperature • Central Nervous
             System Depressants • Cognition • Dose-Response
             Relationship, Drug • Ethanol • Female •
             Injections, Intraperitoneal • Injections, Subcutaneous
             • Maze Learning • Memory, Short-Term •
             Nicotine • Nicotinic Agonists • Rats • Rats,
             Sprague-Dawley • drug effects • drug effects*
             • pharmacology*},
   Abstract = {Nicotine and ethanol are the most widely abused drugs in the
             world. They are very often used and abused together.
             However, little is known about the functional interaction of
             nicotine and ethanol. The current project studied the
             interactive effects of nicotine and ethanol on working
             memory in the eight-arm radial maze. Adult female rats were
             trained on a radial arm maze for 18 sessions to reach
             asymptotic levels of choice accuracy. During the maintenance
             phase of radial arm maze testing, which indexed working
             memory function, the rats were injected with nicotine (0,
             0.15, 0.3, 0.6, and 1.2 mg/kg sc, 20 min before testing)
             with and without ethanol pretreatment (0 or 1.5 g/kg, 16%
             v/v ip, 30 min before testing). All animals received the
             treatments in a counterbalanced order with at least 1 week
             between treatments. Higher doses of nicotine had a
             significant interaction with ethanol in terms of radial arm
             maze choice accuracy. Nicotine plus ethanol coadministration
             precipitated a significant choice accuracy impairment at
             doses that when given alone had no effect on performance. At
             the lower dose range of nicotine, ethanol coadministration
             eliminated the nicotine-induced memory improvement. No
             significant effects were seen with either nicotine or
             ethanol treatment or their interaction on response latency
             in the radial arm maze. The nicotine-ethanol interactive
             effects on memory were compared with the interaction of
             their well-characterized hypothermic effects. Nicotine and
             alcohol, when injected separately or in combination, induced
             hypothermia with no significant interactive effect. This
             study found that ethanol blocked low-dose nicotine-induced
             memory improvement and precipitated memory impairment with
             high-dose nicotine treatment. This interaction may be an
             important consideration for nicotine and ethanol coabuse and
             the possible therapeutic use of nicotinic drugs for memory
             dysfunction.},
   Language = {eng},
   Key = {fds275678}
}

@article{fds216571,
   Author = {AH Rezvani and PJ Bushnell and JM Burkholder and HB Glasgow Jr and ED
             Levin},
   Title = {Specificity of cognitive impairment from Pfiesteria
             piscicida exposure in rats: attention and visual function
             versus behavioral plasticity.},
   Journal = {Neurotoxicology and teratology},
   Volume = {23},
   Number = {6},
   Pages = {609-16},
   Year = {2002},
   Month = {March},
   ISSN = {0892-0362},
   Keywords = {Animals • Attention • Discrimination Learning
             • Female • Injections, Subcutaneous • Maze
             Learning • Pfiesteria piscicida • Photic
             Stimulation • Rats • Rats, Sprague-Dawley •
             drug effects* • pathogenicity*},
   Abstract = {Pfiesteria piscicida is a toxic dinoflagellate that has
             caused massive fish kills in estuaries along the East Coast
             of the United States, and exposure of humans to toxic
             Pfiesteria has been associated with cognitive impairment. A
             visual signal detection task was used to determine the
             possible importance of attentional and visual processes in
             Pfiesteria effects on cognitive function. Adult female rats
             were trained to perform the signal detection task. After
             training, the rats were injected subcutaneously with fish
             culture water containing toxic Pfiesteria (35,600 or 106,800
             cells of Pfiesteria/kg of rat body weight) or with (control)
             fish culture water containing no Pfiesteria. Effects of
             toxic Pfiesteria on maintenance of signal detection behavior
             were assessed for 2 weeks after treatment. Then, the
             signal-response contingencies were reversed. After the
             discrimination was reestablished on the reversed levers, the
             rats received a second dose of toxic Pfiesteria. The rats
             were again tested for 2 weeks, after which a second reversal
             was imposed. Pfiesteria did not affect behavior in the
             signal detection task during 2 weeks of prereversal testing
             after either exposure. However, a significant
             Pfiesteria-induced deficit emerged when the signal-response
             contingencies were reversed. These findings suggest that
             Pfiesteria-induced deficits emerge during periods of
             behavioral transition and not during performance of
             previously learned tasks.},
   Language = {eng},
   Key = {fds216571}
}

@article{fds275662,
   Author = {Rezvani, AH and Parsian, A and Overstreet, DH},
   Title = {The Fawn-Hooded (FH/Wjd) rat: a genetic animal model of
             comorbid depression and alcoholism.},
   Journal = {Psychiatric Genetics},
   Volume = {12},
   Number = {1},
   Pages = {1-16},
   Year = {2002},
   Month = {March},
   ISSN = {0955-8829},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11901354},
   Keywords = {Alcoholism • Animals • Depression • Disease
             Models, Animal • Maze Learning • Phenotype •
             Rats • Rats, Inbred Strains • Restraint, Physical
             • Saccharin • Social Behavior • Stress,
             Psychological • administration & dosage •
             complications • genetics* • physiopathology},
   Abstract = {The Fawn-Hooded (FH/Wjd) rat is an inbred strain of rat that
             has been reported to exhibit both high immobility in the
             forced swim test and high voluntary ethanol intake, measures
             that have been periodically linked with depression and
             alcoholism in humans. The present paper will first present a
             survey of the literature and previously unpublished findings
             that bear on the question of whether FH/Wjd rats should be
             considered genetic animal models of depression and
             alcoholism. Subsequently, behavioral studies of the FH/Wjd
             rats, the non-drinking ACI/N strain, and their F1 and F2
             intercrosses will be described. Under free choice
             conditions, the FH/Wjd rat drinks up to 6 g/kg 10% ethanol
             per day. This intake was sufficient to render the rats
             tolerant to the hypothermic effects of injected ethanol (2.5
             g/kg). Rats that had been voluntarily drinking for at least
             6 weeks also exhibited withdrawal-induced anxiety in the
             social interaction, elevated plus maze, and ultrasonic
             vocalization tasks. The FH/Wjd rat exhibits a 25-30%
             increase in alcohol intake when the alcohol is returned
             after a 24-h period of deprivation. It responds to drugs
             that are effective in humans with a reduction in alcohol
             intake. Therefore, the FH/Wjd rat meets most of the criteria
             for an animal model of alcoholism. Chronic antidepressant
             treatments correct several of the abnormalities exhibited by
             the FH/Wjd rats, including the exaggerated immobility in the
             forced swim test. Therefore, the FH/Wjd rats also fulfill
             some of the criteria for an animal model of depression. On
             the contrary, inbred ACI/N rats do not drink much alcohol
             voluntarily and are quite active in the forced swim test.
             The FH/Wjd and ACI/N rats were intercrossed to obtain the F1
             and F2 progenies, which were then tested for alcohol intake
             and immobility. Alcohol intake and immobility were
             distributed in different patterns in the F1 and F2
             progenies. Alcohol intake was intermediate in the F1
             progeny, while immobility was closer to the FH/Wjd parents.
             In the F2 progeny, chi-square analyses indicated that the
             distributions were significantly different. In addition,
             there were no significant litter effects, indicating that
             maternal effects did not appear to occur. There were also no
             significant differences among rats with different coat
             colors, suggesting that the Fawn-Hooded phenotype can be
             separated from the measures of alcohol intake and
             immobility. We conclude that the FH/Wjd rat is a genetic
             animal model of depression and alcoholism, but that the two
             measures reflective of these states are under separate
             genetic controls.},
   Language = {eng},
   Doi = {10.1097/00041444-200203000-00001},
   Key = {fds275662}
}

@article{fds275676,
   Author = {Rezvani, AH and Bushnell, PJ and Burkholder, JM and Glasgow, HB and Levin, ED},
   Title = {Specificity of cognitive impairment from Pfiesteria
             piscicida exposure in rats: attention and visual function
             versus behavioral plasticity.},
   Journal = {Neurotoxicology and Teratology},
   Volume = {23},
   Number = {6},
   Pages = {609-616},
   Year = {2001},
   Month = {November},
   ISSN = {0892-0362},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11792529},
   Abstract = {Pfiesteria piscicida is a toxic dinoflagellate that has
             caused massive fish kills in estuaries along the East Coast
             of the United States, and exposure of humans to toxic
             Pfiesteria has been associated with cognitive impairment. A
             visual signal detection task was used to determine the
             possible importance of attentional and visual processes in
             Pfiesteria effects on cognitive function. Adult female rats
             were trained to perform the signal detection task. After
             training, the rats were injected subcutaneously with fish
             culture water containing toxic Pfiesteria (35,600 or 106,800
             cells of Pfiesteria/kg of rat body weight) or with (control)
             fish culture water containing no Pfiesteria. Effects of
             toxic Pfiesteria on maintenance of signal detection behavior
             were assessed for 2 weeks after treatment. Then, the
             signal-response contingencies were reversed. After the
             discrimination was reestablished on the reversed levers, the
             rats received a second dose of toxic Pfiesteria. The rats
             were again tested for 2 weeks, after which a second reversal
             was imposed. Pfiesteria did not affect behavior in the
             signal detection task during 2 weeks of prereversal testing
             after either exposure. However, a significant
             Pfiesteria-induced deficit emerged when the signal-response
             contingencies were reversed. These findings suggest that
             Pfiesteria-induced deficits emerge during periods of
             behavioral transition and not during performance of
             previously learned tasks.},
   Key = {fds275676}
}

@article{fds275661,
   Author = {Gordon, CJ and Rezvani, AH},
   Title = {Genetic selection of rats with high and low body
             temperatures.},
   Journal = {Journal of Thermal Biology},
   Volume = {26},
   Number = {3},
   Pages = {223-229},
   Year = {2001},
   Month = {June},
   ISSN = {0306-4565},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11240229},
   Abstract = {Body (core) temperature (T(c)) directly affects all
             biological processes, including sensitivity to toxic
             chemicals, development, aging, and drug metabolism. To
             understand how T(c) affects these processes it is necessary
             to alter T(c) independently of other physiological
             processes. The purpose of this study was to determine
             whether selective breeding techniques can be used to develop
             lines of rats with hyperthermic and hypothermic T(c)'s. T(c)
             and motor activity of 24 female and 23 male rats (parental
             line) of the NIH heterogenous stock were monitored by
             telemetry for 96h at a T(a) of 22 degrees C. The mean 24h
             T(c) of the male and female rats was 37.3 degrees C with a
             range of 37-38.2 degrees C. T(c) was not correlated with
             motor activity or body weight. Pairs with the lowest and
             highest T(c)'s were selected for breeding. The F1 generation
             consisted of 10 offspring from the hyperthermic group and 20
             from the hypothermic group. They were implanted with
             transmitters at 60d of age. T(c) of rats derived from the
             hyperthermic parental line had a significantly warmer T(c)
             than the rats derived from the hypothermic parental line.
             Motor activity was significantly higher in the hyperthermic
             F1 males and hypothermic F1 females. Breeding of
             hyperthermic and hypothermic rats has shown that adult
             offspring of the fourth generation maintain significantly
             different core temperatures but have similar patterns of
             motor activity. The results demonstrate that T(c) is
             heritable and that it should be feasible to develop lines of
             rats that regulate T(c) above or below normal.},
   Language = {ENG},
   Key = {fds275661}
}

@article{fds275677,
   Author = {Rezvani, AH and Levin, ED},
   Title = {Cognitive effects of nicotine.},
   Journal = {Biological Psychiatry},
   Volume = {49},
   Number = {3},
   Pages = {258-267},
   Year = {2001},
   Month = {February},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11230877},
   Keywords = {Adult • Aged • Alzheimer Disease • Animals
             • Cognition Disorders • Hippocampus • Humans
             • Neuropsychological Tests* • Nicotine •
             Receptors, Nicotinic • Treatment Outcome • drug
             effects • drug therapy* • therapeutic
             use*},
   Abstract = {Nicotine and other nicotinic agonists have been found to
             improve performance on attention and memory tasks. Clinical
             studies using nicotine skin patches have demonstrated the
             efficacy of nicotine in treating cognitive impairments
             associated with Alzheimer's disease, schizophrenia, and
             attention-deficit/hyperactivity disorder. Experimental
             animal studies have demonstrated the persistence of
             nicotine-induced working memory improvement with chronic
             exposure, in addition to the efficacy of a variety of
             nicotinic agonists. Mechanistic studies have found that
             alpha7 and alpha4beta2 nicotinic receptors in the
             hippocampus are critical for nicotinic involvement in
             cognitive function. Clinical and experimental animal studies
             provide mutually supporting information for the development
             of novel nicotinic therapies for cognitive
             dysfunction.},
   Language = {eng},
   Doi = {10.1016/s0006-3223(00)01094-5},
   Key = {fds275677}
}

@article{fds275660,
   Author = {Matthews, DB and Overstreet, DH and Rezvani, AH and Devaud, LL and Morrow, AL},
   Title = {Effects of sweetened ethanol solutions on ethanol
             self-administration and blood ethanol levels.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {68},
   Number = {1},
   Pages = {13-21},
   Year = {2001},
   Month = {January},
   ISSN = {0091-3057},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11274703},
   Keywords = {Alcohol Drinking • Animals • Bicuculline •
             Central Nervous System Depressants • Convulsants •
             Dose-Response Relationship, Drug • Ethanol • Male
             • Rats • Rats, Sprague-Dawley • Seizures
             • Self Administration • Taste • blood •
             chemically induced • drug effects* • pharmacology
             • pharmacology* • prevention & control •
             psychology*},
   Abstract = {The enhancement of voluntary self-administration of ethanol
             by sucrose or saccharin was tested in conjunction with
             measurements of blood ethanol levels. Adult male rats were
             given access to both tap water and one of five solutions:
             0.125% saccharin, 10% sucrose, ethanol, saccharin+ethanol,
             or sucrose+ethanol. The rats receiving the sucrose+ethanol
             solution drank consistently more ethanol (>5 g/kg/day) than
             did the rats receiving the saccharin+ethanol solution (<3
             g/kg/day) or ethanol only (<2 g/kg/day). Both sweetened
             solutions produced higher ethanol consumption during these
             periods than ethanol alone. However, no significant
             differences in blood ethanol levels were found between the
             sucrose+ethanol and saccharin+ethanol conditions, when
             tested at different intervals on Day 44 or Day 45 of ethanol
             consumption. Following 45 days of consumption, no change in
             the bicuculline seizure threshold was observed in the
             ethanol-consuming rats compared to the controls. In a
             separate study using 90 naive rats, rats were gavaged with
             ethanol (1, 2, or 3 g/kg) containing either 10% sucrose
             (n=10 for each dose of ethanol), 0.125% saccharin (n=10 for
             each dose of ethanol), or ethanol alone (n=10 for each dose
             of ethanol), and blood was collected from the tip of the
             tail 30, 60, 180, 300, and 540 min later and analyzed for
             ethanol concentrations. Sucrose significantly decreased the
             resultant blood ethanol levels at several time points
             following gavage. These results indicate that sucrose can
             significantly alter blood ethanol levels and that chronic
             self-administration of a sweetened ethanol solution for 6
             weeks does not produce ethanol dependence.},
   Language = {eng},
   Doi = {10.1016/s0091-3057(00)00458-5},
   Key = {fds275660}
}

@article{fds135625,
   Title = {1. Rezvani A.H., and Levin E.D. Cognitive effects of
             nicotine. Biological Psychiatry 49: 258-267,
             2001.},
   Year = {2001},
   Key = {fds135625}
}

@article{fds135626,
   Title = {3. Gordon C.J., and Rezvani A.H. Genetic selection of rats
             with high and low body temperatures. J. Thermal Biology
             26:23-29, 2001.},
   Year = {2001},
   Key = {fds135626}
}

@article{fds135627,
   Title = {6. Levin ED, Rezvani AH. Nicotine involvement in memory
             function of rats. In: Nicotinic receptors in the nervous
             system Levin E.D. ed. Pp167-178, CRC Press,
             2001.},
   Year = {2001},
   Key = {fds135627}
}

@article{fds135628,
   Title = {2. Matthews D.B., Overstreet D.H. Rezvani A.H., Devaud L.L.,
             and Morrow A.L. Effects of sweetened ethanol solutions on
             ethanol self-administration and blood ethanol levels.
             Pharmacol. Biochem. Behav. 68:13-21, 2001.},
   Year = {2001},
   Key = {fds135628}
}

@article{fds135629,
   Title = {4. Rezvani AH, Bushnell PJ, Burkholder JM, Glasgow HB, and
             Levin ED. Specificity of cognitive impairment from
             Pfiesteria piscicida exposure in rats: Attention and visual
             function vs behavioral plasticity. Neurotoxicology and
             Teratology 23:609-616 2001.},
   Year = {2001},
   Key = {fds135629}
}

@article{fds275674,
   Author = {Levin, ED and Mead, T and Rezvani, AH and Rose, JE and Gallivan, C and Gross, R},
   Title = {The nicotinic antagonist mecamylamine preferentially
             inhibits cocaine vs. food self-administration in
             rats.},
   Journal = {Physiology & Behavior},
   Volume = {71},
   Number = {5},
   Pages = {565-570},
   Year = {2000},
   Month = {December},
   ISSN = {0031-9384},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11239676},
   Keywords = {Animals • Cocaine • Conditioning, Operant •
             Dopamine Uptake Inhibitors • Eating • Female
             • Food • Mecamylamine • Nicotinic Antagonists
             • Rats • Rats, Sprague-Dawley • Reinforcement
             (Psychology) • Self Administration •
             administration & dosage • drug effects • drug
             effects* • pharmacology*},
   Abstract = {Nicotinic acetylcholine systems play important roles in
             addiction, and nicotinic receptor stimulation stimulates
             dopamine release while the nicotinic antagonist mecamylamine
             reduces it. Reid et al. [Neuropsychopharmacology 20 (1999)
             297.] recently found in human cocaine addicts that
             mecamylamine reduced cue-elicited cocaine craving. The
             current study assessed the impact of mecamylamine on cocaine
             self-administration in rats. Female Sprague-Dawley rats
             (N=7) were implanted with intravenous (iv) catheters and
             trained to lever press for cocaine (0.32 mg/kg/infusion FR-1
             with a 60-s timeout) in 45-min sessions. After 2 weeks of
             training, the rats were injected with saline or mecamylamine
             (1, 2, or 4 mg/kg sc) 10 min before the session. They
             received the same dose for 1 week with 1 week of uninjected
             testing between doses. Mecamylamine, compared to saline,
             significantly (P<.05) reduced the number of cocaine
             infusions per session with each of these doses. This effect
             did not appear to be due to a generalized reduction in
             behavioral activity. Another set of female Sprague-Dawley
             rats (N=8) were trained to lever press for food
             reinforcement. In these rats, the 1 and 2-mg/kg mecamylamine
             doses had no effect on food self-administration. Significant
             reductions in food self-administration were not seen unless
             the high dose of 4-mg/kg mecamylamine was used. Nicotinic
             antagonist treatment reduces cocaine self-administration in
             rats at doses that do not cause generalized effects on
             food-reinforced responding. Nicotinic antagonistic treatment
             may be a useful new approach to treat cocaine
             addiction.},
   Language = {eng},
   Doi = {10.1016/s0031-9384(00)00382-6},
   Key = {fds275674}
}

@article{fds216532,
   Author = {ED Levin and AH Rezvani and NC Christopher and HB Glasgow Jr and NJ
             Deamer-Melia, JM Burkholder and VC Moser and K
             Jensen},
   Title = {Rapid neurobehavioral analysis of Pfiesteria piscicida
             effects in juvenile and adult rats.},
   Journal = {Neurotoxicology and teratology},
   Volume = {22},
   Number = {4},
   Pages = {533-40},
   Year = {2000},
   Month = {October},
   ISSN = {0892-0362},
   Keywords = {Aging • Animals • Behavior, Animal • Female
             • Male • Maze Learning • Motor Activity
             • Pfiesteria piscicida* • Protozoan Infections,
             Animal • Rats • Rats, Sprague-Dawley •
             physiology • physiology* • physiopathology*},
   Abstract = {The estuarine dinoflagellate Pfiesteria piscicida is known
             to kill fish and has been associated with neurocognitive
             deficits in humans. We have developed a rat model to
             demonstrate that exposure to Pfiesteria causes significant
             learning impairments. This has been repeatedly seen as a
             choice accuracy impairment during radial-arm maze learning.
             Pfiesteria-induced effects were also seen in a locomotor
             activity test in the figure-8 apparatus. The current studies
             used the short-term radial-arm maze acquisition, the
             figure-8 activity test, and the functional observational
             battery (FOB) to assess Pfiesteria-induced neurobehavioral
             effects in adult and juvenile rats. In study 1, the
             neurobehavioral potency of three different Pfiesteria
             cultures (Pf 113, Pf 728, and Pf Vandermere) was assessed.
             Ninety-six (12 per group) adult female Sprague-Dawley rats
             were injected subcutaneously with a single dose of
             Pfiesteria taken from aquarium-cultured Pfiesteria (35,600
             or 106,800 Pfiesteria cells per kilogram of rat body
             weight). One control group (N = 12) was injected with saline
             and one (N = 12) with aquarium water not containing
             Pfiesteria. All three of the Pfiesteria samples (p < 0.05)
             impaired choice accuracy over the first six sessions of
             training. At the time of the radial-arm maze choice accuracy
             impairment, no overt Pfiesteria-related effects were seen
             using an FOB, indicating that the Pfiesteria-induced choice
             accuracy deficit was not due to generalized debilitation. In
             the figure-8 apparatus, Pfiesteria treatment caused a
             significant decrease in mean locomotor activity. In study 2,
             the neurobehavioral effects of the Pf 728 sample type were
             assessed in juvenile rats. Twenty-four day-old male and
             female rats were injected with 35,600 or 106,800 Pf-728
             Pfiesteria cells per kilogram of rat body weight. As with
             adult females, the juvenile rats showed a significant
             impairment in radial-arm maze choice accuracy. No changes in
             locomotor activity or the FOB were detected in the juvenile
             rats. Furthermore, there were no differences between male
             and female rats in the Pfiesteria-induced choice accuracy
             impairment. Pfiesteria effects on choice accuracy in the
             radial-arm maze in rats constitute a critical component of
             the model of Pfiesteria toxicity, because the hallmark of
             Pfiesteria toxicity in humans is cognitive dysfunction. Our
             finding that analysis of the first six sessions of
             radial-arm maze testing is sufficient for determining the
             effect means that this test will be useful as a rapid screen
             for identifying the critical neurotoxin(s) of Pfiesteria in
             future studies.},
   Language = {eng},
   Key = {fds216532}
}

@article{fds275675,
   Author = {Levin, ED and Rezvani, AH and Christopher, NC and Glasgow, HB and Deamer-Melia, NJ and Burkholder, JM and Moser, VC and Jensen,
             K},
   Title = {Rapid neurobehavioral analysis of Pfiesteria piscicida
             effects in juvenile and adult rats.},
   Journal = {Neurotoxicology and Teratology},
   Volume = {22},
   Number = {4},
   Pages = {533-540},
   Year = {2000},
   Month = {July},
   ISSN = {0892-0362},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/10974591},
   Abstract = {The estuarine dinoflagellate Pfiesteria piscicida is known
             to kill fish and has been associated with neurocognitive
             deficits in humans. We have developed a rat model to
             demonstrate that exposure to Pfiesteria causes significant
             learning impairments. This has been repeatedly seen as a
             choice accuracy impairment during radial-arm maze learning.
             Pfiesteria-induced effects were also seen in a locomotor
             activity test in the figure-8 apparatus. The current studies
             used the short-term radial-arm maze acquisition, the
             figure-8 activity test, and the functional observational
             battery (FOB) to assess Pfiesteria-induced neurobehavioral
             effects in adult and juvenile rats. In study 1, the
             neurobehavioral potency of three different Pfiesteria
             cultures (Pf 113, Pf 728, and Pf Vandermere) was assessed.
             Ninety-six (12 per group) adult female Sprague-Dawley rats
             were injected subcutaneously with a single dose of
             Pfiesteria taken from aquarium-cultured Pfiesteria (35,600
             or 106,800 Pfiesteria cells per kilogram of rat body
             weight). One control group (N = 12) was injected with saline
             and one (N = 12) with aquarium water not containing
             Pfiesteria. All three of the Pfiesteria samples (p < 0.05)
             impaired choice accuracy over the first six sessions of
             training. At the time of the radial-arm maze choice accuracy
             impairment, no overt Pfiesteria-related effects were seen
             using an FOB, indicating that the Pfiesteria-induced choice
             accuracy deficit was not due to generalized debilitation. In
             the figure-8 apparatus, Pfiesteria treatment caused a
             significant decrease in mean locomotor activity. In study 2,
             the neurobehavioral effects of the Pf 728 sample type were
             assessed in juvenile rats. Twenty-four day-old male and
             female rats were injected with 35,600 or 106,800 Pf-728
             Pfiesteria cells per kilogram of rat body weight. As with
             adult females, the juvenile rats showed a significant
             impairment in radial-arm maze choice accuracy. No changes in
             locomotor activity or the FOB were detected in the juvenile
             rats. Furthermore, there were no differences between male
             and female rats in the Pfiesteria-induced choice accuracy
             impairment. Pfiesteria effects on choice accuracy in the
             radial-arm maze in rats constitute a critical component of
             the model of Pfiesteria toxicity, because the hallmark of
             Pfiesteria toxicity in humans is cognitive dysfunction. Our
             finding that analysis of the first six sessions of
             radial-arm maze testing is sufficient for determining the
             effect means that this test will be useful as a rapid screen
             for identifying the critical neurotoxin(s) of Pfiesteria in
             future studies.},
   Key = {fds275675}
}

@article{fds275673,
   Author = {Levin, ED and Rezvani, AH},
   Title = {Development of nicotinic drug therapy for cognitive
             disorders.},
   Journal = {European Journal of Pharmacology},
   Volume = {393},
   Number = {1-3},
   Pages = {141-146},
   Year = {2000},
   Month = {March},
   ISSN = {0014-2999},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/10771007},
   Keywords = {Adult • Alzheimer Disease • Animals •
             Attention • Attention Deficit Disorder with
             Hyperactivity • Cognition Disorders • Disease
             Models, Animal • Drug Design • Humans •
             Learning • Memory • Nicotine • Nicotinic
             Agonists • Rats • Schizophrenia • Smoking
             • drug effects • drug therapy • drug therapy*
             • pharmacology • therapeutic use*},
   Abstract = {Nicotine, as well as other nicotinic drugs, may provide
             useful therapeutic treatment for a variety of cognitive
             impairments including those found in Alzheimer's disease,
             schizophrenia and attention deficit hyperactivity disorder
             (ADHD). We have found that nicotine skin patches
             significantly improve attentional performance in people with
             these disease states as well as normal nonsmoking adults.
             Animal models are critical for determining the
             neurobehavioral bases for nicotinic effects on cognitive
             function. We have found in lesion and local infusion studies
             with rats that the hippocampus is an important substrate for
             nicotinic effects on working memory function. Both alpha7
             and alpha4beta2 nicotinic receptors in the hippocampus are
             involved. Further work has investigated the relationship of
             nicotinic systems with dopaminergic and glutaminergic
             systems in the basis of cognitive function. Nicotine has
             proven to be a useful prototypic compound for the family of
             nicotinic compounds. It produces cognitive improvements in
             both animal models and clinical populations. Recent work
             with more selective nicotinic receptor agonists and
             antagonists in animal models is providing important
             information concerning the neural mechanisms for nicotinic
             involvement in cognitive function and opening avenues for
             development of safe and effective nicotinic treatments for
             clinical use.},
   Language = {eng},
   Key = {fds275673}
}

@article{fds275656,
   Author = {Farren, CK and Rezvani, AH and Overstreet, D and O'Malley,
             S},
   Title = {Combination pharmacotherapy in alcoholism: a novel treatment
             approach.},
   Journal = {Cns Spectrums},
   Volume = {5},
   Number = {2},
   Pages = {70-76},
   Year = {2000},
   Month = {February},
   ISSN = {1092-8529},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18297000},
   Abstract = {Combination pharmacotherapy has proven effective in a number
             of psychiatric disorders, including depression and
             schizophrenia. However, compared with other affective
             disorders, few studies have explored the use of combination
             therapy in alcoholism, and the majority have been limited to
             animal models. There is evidence to support a role for
             combination therapy in alcoholism. For example, several
             neurochemical systems, including the dopaminergic,
             serotonergic, and opioidergic, appear to affect alcohol
             intake. Studies in several different types of
             alcohol-preferring rats have suggested that coadministration
             of agents to target more than one of these systems
             simultaneously may produce beneficial effects on alcohol
             intake, while avoiding problematic effects, such as
             alterations in food or water intake. Data from preliminary
             clinical studies have shown trends toward combination
             therapy reducing alcohol intake in humans. While such
             findings are encouraging, they must be explored further in
             larger, randomized, double-blind trials.},
   Language = {eng},
   Key = {fds275656}
}

@article{fds275657,
   Author = {Rezvani, AH and Overstreet, DH and Mason, GA and Janowsky, DS and Hamedi, M and Clark, E and Yang, Y},
   Title = {Combination pharmacotherapy: a mixture of small doses of
             naltrexone, fluoxetine, and a thyrotropin-releasing hormone
             analogue reduces alcohol intake in three strains of
             alcohol-preferring rats.},
   Journal = {Alcohol and Alcoholism (Oxford, Oxfordshire)},
   Volume = {35},
   Number = {1},
   Pages = {76-83},
   Year = {2000},
   Month = {January},
   ISSN = {0735-0414},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/10684782},
   Keywords = {Alcohol Drinking • Animals • Drug Therapy,
             Combination • Fluoxetine • Naltrexone •
             Narcotic Antagonists • Nootropic Agents • Rats
             • Rats, Wistar • Serotonin Uptake Inhibitors
             • Thyrotropin-Releasing Hormone • analogs &
             derivatives • drug therapy* • genetics •
             therapeutic use • therapeutic use*},
   Abstract = {It is common to treat some diseases with more than one
             medication simultaneously. Since more than one
             neurotransmitter system is involved in alcohol-seeking
             behaviour, then a therapeutic approach that targets more
             than one system should be more effective in reducing alcohol
             intake than one addressing a single system. To test this
             hypothesis, we compared the efficacy of low doses of
             individual drugs reported to reduce voluntary alcohol
             drinking to the efficacy of a mixture of these agents at the
             same low doses in reducing alcohol intake in three strains
             of alcohol-preferring rats (P, HAD, and Fawn-Hooded). After
             establishment of a stable baseline for alcohol intake in a
             continuous access paradigm, each rat received separate
             single i.p. injections of relatively low doses of either
             naltrexone (2.0 mg/kg), fluoxetine (1.0 mg/kg), the
             thyrotropin-releasing hormone analogue TA-0910 (0.2 mg/kg),
             a mixture of all three drugs, or the vehicle at 09:30. Each
             rat received all treatments, with an inter-injection washout
             period of at least 3 days. Alcohol and water intakes were
             measured at 6 and 24 h, and food intake was measured at 24
             h, after the injection. Our results show that individual
             drugs did not significantly affect food, water, or alcohol
             intake. However, the mixture significantly reduced alcohol
             intake in all three strains, but had no effect on food
             intake. Similar results were obtained when the HAD rats
             received an oral dose of the individual drugs or the
             mixture. When P rats were given an i.p. injection of the
             mixture for 10 consecutive days, there was a continued
             suppressing effect. These findings show that a combination
             treatment designed to target simultaneously serotonergic,
             dopaminergic, and opioidergic systems can reduce alcohol
             intake, even though the doses of the individual drugs in the
             mixture are relatively low and ineffective when given
             singly.},
   Language = {eng},
   Key = {fds275657}
}

@article{fds275658,
   Author = {Tizabi, Y and Rezvani, AH and Russell, LT and Tyler, KY and Overstreet,
             DH},
   Title = {Depressive characteristics of FSL rats: Involvement of
             central nicotinic receptors},
   Journal = {Pharmacology Biochemistry and Behavior},
   Volume = {66},
   Number = {1},
   Pages = {73-77},
   Year = {2000},
   url = {http://dx.doi.org/10.1016/S0091-3057(00)00236-7},
   Abstract = {Antidepressant effects of acute or chronic nicotine
             treatments in swim test immobility of Flinders sensitive
             line (FSL) rats, an animal model of depression, were
             recently demonstrated (Tizabi et al. Psychopharmacology
             142:193, 1999). In the present study we sought to determine
             whether the antidepressant effects of nicotine could be
             blocked by the nicotinic antagonist, mecamylamine (MEC).
             Moreover, the effects of chronic nicotine treatment on
             [3H]cytisine binding in discrete brain regions of FSL and
             their control Flinders resistant line (FRL) rats were also
             evaluated. Adult male FSL rats were treated with MEC (0.5
             mg/kg) 20 min prior to an acute or chronic nicotine
             administration. MEC by itself did not affect the immobility
             in swim test. However, it completely blocked the acute or
             chronic nicotine effects. Daily nicotine injection (0.4
             mg/kg/day for 14 days) resulted in an increase in
             [3H]cytisine binding primarily in the FRL rats. An increase
             in nicotinic receptor binding following chronic nicotine
             administration is believed to reflect desensitization of
             these receptors. These findings, coupled with previous
             observation of higher basal nicotinic receptors in FSL rats,
             further support the involvement of central nicotinic
             receptors in depressive characteristics of these rats.
             Moreover, the data suggest therapeutic potential for
             selective nicotinic receptor agonists in depressive
             disorders. (C) 2000 Elsevier Science Inc.},
   Doi = {10.1016/S0091-3057(00)00236-7},
   Key = {fds275658}
}

@article{fds275659,
   Author = {Parsian, A and Overstreet, DH and Rezvani, A},
   Title = {Independent segregation of alcohol intake and immobility in
             F2 progeny from FH/ ACI intercross},
   Journal = {American Journal of Medical Genetics. Part B,
             Neuropsychiatric Genetics : the Official Publication of the
             International Society of Psychiatric Genetics},
   Volume = {96},
   Number = {4},
   Pages = {560-},
   Year = {2000},
   ISSN = {1552-4841},
   Abstract = {The inbred Fawn-Hooded (FH/Wjd) strain of rats not only
             drinks substantial amounts of alcohol voluntarily compared
             to the inbred ACI (ACI/N) strain, they also exhibit
             exaggerated immobility in the forced swim test (measurement
             for depression), have high saccharin and total fluid
             intakes. Whether these differences are due to the
             pleiotropic effects of the same genes or due to the effects
             of independent genes can be evaluated, in part, by
             determining how these variables segregate in the F2
             population. A total of 144 F2 (74 males and 70 females) rats
             from a cross between the FH/ Wjd strain and the ACI/N strain
             were tested with a behavioral battery. Analysis of variance
             determined that there were no litter effects on alcohol
             intake, nor did this measure vary with coat color. A
             correlation matrix was established for the 7 variables
             measured: water intake, forced alcohol intake, voluntary
             alcohol intake, alcohol preference, saccharin intake, total
             fluid intake, and immobility in the forced swim test.
             Voluntary alcohol intake was highly correlated (r = +0.914)
             with alcohol preference but was not significantly correlated
             with any other variables. Immobility was not significantly
             correlated with any of the other variables. Saccharin was
             significantly correlated with total fluid intake and forced
             alcohol intake. These findings of independent segregation of
             voluntary alcohol intake, saccharin intake and immobility in
             the F2 population of FH/ACI rats suggests that the
             differences in the parental strains may be the consequence
             of independent genetic factors. A QTL study of these animals
             could confirm this conclusion.},
   Key = {fds275659}
}

@article{fds216540,
   Author = {AH Rezvani and DH Overstreet and Y Yang and E Clark
             Jr},
   Title = {Attenuation of alcohol intake by extract of Hypericum
             perforatum (St. John's Wort) in two different strains of
             alcohol-preferring rats.},
   Journal = {Alcohol and alcoholism (Oxford, Oxfordshire)},
   Volume = {34},
   Number = {5},
   Pages = {699-705},
   Year = {1999},
   Month = {November},
   ISSN = {0735-0414},
   Keywords = {Alcohol Deterrents • Alcohol Drinking • Animals
             • Central Nervous System Depressants • Drug
             Evaluation, Preclinical • Eating • Ethanol •
             Hypericum • Phytotherapy* • Plant Extracts •
             Plants, Medicinal* • Rats • administration &
             dosage* • drug effects • drug therapy* •
             genetics • therapeutic use • therapeutic
             use*},
   Abstract = {Extract of the common plant Hypericum perforatum L. (St
             John's Wort, SJW) has been used successfully for the
             treatment of mild to moderate depression since ancient times
             and has recently been studied clinically. Depression and
             alcoholism have some neurochemical similarities, such as low
             brain serotonin activities. Thus, we hypothesized that SJW
             extract, which contains 0.22% hypericin and 4.05%
             hyperforin, also may be effective in suppressing alcohol
             intake. To test this hypothesis, the effects of SJW extract
             on voluntary alcohol intake were studied in two different
             genetic animal models of human alcoholism: fawn-hooded (FH)
             and high-alcohol drinking (HAD) rats. FH and HAD rats
             received a single oral administration (5 ml/kg) of either
             vehicle or one of the five doses (100, 200, 400, 600, and
             800 mg/kg) of SJW extract. The oral administration of SJW
             extract significantly (P < 0.0001) reduced alcohol intake in
             both FH and HAD rats. In a third study, FH rats did not
             develop tolerance to the suppressant effects of SJW on
             alcohol intake and preference following oral administration
             of (400 mg/kg) of the extract for 15 consecutive days. These
             promising findings suggest that SJW extract should be
             evaluated clinically as a potential therapeutic agent in the
             treatment of alcoholism.},
   Language = {eng},
   Key = {fds216540}
}

@article{fds275655,
   Author = {Overstreet, DH and Kampov-Polevoy, AB and Rezvani, AH and Braun, C and Bartus, RT and Crews, FT},
   Title = {Suppression of alcohol intake by chronic naloxone treatment
             in P rats: tolerance development and elevation of opiate
             receptor binding.},
   Journal = {Alcoholism, Clinical and Experimental Research},
   Volume = {23},
   Number = {11},
   Pages = {1761-1771},
   Year = {1999},
   Month = {November},
   ISSN = {0145-6008},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/10591592},
   Keywords = {Alcohol Drinking • Analgesics, Opioid • Animals
             • Dose-Response Relationship, Drug • Drug
             Tolerance • Enkephalin, Ala(2)-MePhe(4)-Gly(5)- •
             Feasibility Studies • Male • Naloxone •
             Narcotic Antagonists • Rats • Receptors, Opioid,
             mu • administration & dosage* • drug effects
             • drug therapy* • metabolism • metabolism*
             • pharmacology • physiology*},
   Abstract = {BACKGROUND: This study was planned to determine the
             feasibility of using a slow release naloxone preparation to
             treat alcoholism, because compliance with medication is a
             significant problem in alcoholics. METHODS: Experiments were
             performed in alcohol-preferring P rats maintained either on
             continuous access or on limited access (1 hr/day) to alcohol
             with water and food provided ad libitum. Naloxone (Nx) was
             administered either by twice daily subcutaneous injections
             or by slow release (1.1 mg/kg/hr) osmotic minipump. In
             limited access experiments, Nx was injected immediately
             before access to alcohol. RESULTS: An initial experiment
             estimated the dose-effect curve for Nx subcutaneous
             suppression on alcohol intake. Nx (2.5-20 mg/kg) had a
             stronger effect during the first 2 hr after injection (ED50
             = 2.1 mg/kg); however, the effect was more modest on 24-hr
             consumption. Similar results were found with chronic Nx
             treatment. Low doses of Nx (0.5 and 2.0 mg/kg) injected
             immediately before limited access to alcohol produced almost
             complete suppression of alcohol intake for at least 14
             consecutive days. However, 14 days of treatment with 26
             mg/kg/day by minipump or injection produced an initial 50%
             suppression of 24-hr alcohol intake with the gradual
             development of tolerance. An acute challenge with Nx
             immediately after the pumps were scheduled to be empty
             provided additional evidence of tolerance development in
             chronically Nx-treated rats. Brain micro-opiate receptors,
             estimated autoradiographically by using the ligand
             [3H][D-Ala2,N-Me-Phe4, Gly-ol5][tyrosyl-3,5-3H]-enkephalin,
             showed that rats chronically exposed to Nx and showing
             tolerance to Nx suppression of drinking exhibited 17% to
             250% increases in [3H][D-Ala2,N-Me-Phe4,
             Gly-ol5][tyrosyl-3,5-3H]-enkephalin binding. CONCLUSIONS:
             High doses of Nx are required to suppress continuous access
             alcohol consumption in P rats, and tolerance develops to the
             ethanol consumption-suppressing effect of Nx that may be
             related to increases in micro-opiate receptors.},
   Language = {eng},
   Key = {fds275655}
}

@article{fds275650,
   Author = {Overstreet, DH and Lee, DYW and Chen, YT and Rezvani, AH and Schuck,
             P},
   Title = {Chinese herb may help to treat alchohol addiction:
             Commentary},
   Journal = {Forschende Komplementarmedizin},
   Volume = {6},
   Number = {4},
   Pages = {226-227},
   Year = {1999},
   Month = {October},
   ISSN = {1021-7096},
   Key = {fds275650}
}

@article{fds216579,
   Author = {DH Overstreet and AH Rezvani and A Parsian},
   Title = {Behavioural features of alcohol-preferring rats: focus on
             inbred strains.},
   Journal = {Alcohol and alcoholism (Oxford, Oxfordshire)},
   Volume = {34},
   Number = {3},
   Pages = {378-85},
   Year = {1999},
   Month = {September},
   ISSN = {0735-0414},
   Keywords = {Alcohol Drinking • Animals • Behavior, Animal
             • Choice Behavior • Ethanol • Factor
             Analysis, Statistical • Male • Maze Learning
             • Phenylalanine • Rats • Rats, Inbred Strains
             • Saccharin • drug effects • drug effects*
             • pharmacology • pharmacology* • physiology*
             • psychology*},
   Abstract = {A recent study conducted a factor analysis on 18 behavioural
             measures obtained from four alcohol-preferring and five
             alcohol-non-preferring rat lines/strains. It was concluded
             that variables such as saccharin intake, ultrasonic
             vocalizations following an air puff, and defaecation in an
             open field were associated with voluntary and forced alcohol
             consumption. In contrast, measures such as time immobile in
             the forced swim test and time spent in the open arms of the
             elevated plus maze were not consistently associated with
             voluntary alcohol intake. The present study focuses on
             alcohol intake and related measures in four inbred strains
             of Fawn-Hooded (FH) rats that differ in voluntary alcohol
             intake and the ACI/N inbred rat strain, which voluntarily
             consumes very little alcohol. FH rats inbred by Jean Dodds
             (FH/Wjd) drank significantly more alcohol than FH rats
             inbred by Gordon Harrington (FH/Har) or selectively inbred
             by Abraham Provoost (FHH/Eur and FHL/EUR). In contrast, only
             the FH/Har strain was active in the forced swim test,
             suggesting that immobility and voluntary alcohol intake may
             be influenced by different genetic factors. The FH/Wjd rats
             were also much more immobile than the ACI/N rats in the
             forced swim test and drank almost 10 times as much alcohol
             voluntarily. Comparing the two parental lines with
             reciprocal F1 crosses revealed that alcohol consumption was
             influenced largely by additive genetic factors (F1 progeny
             had intermediate scores), whereas immobility was also
             influenced by dominance genetic factors (F progeny resembled
             the FH/Wjd parent). Preliminary analysis of 43 F2 progeny
             indicated that alcohol intake and immobility were not
             correlated. Thus, immobility in the forced swim test and
             high voluntary consumption of alcohol, two prominent
             features of the FH/Wjd rat strain which may be related to
             its serotonergic dysfunction, appear to be mediated by
             different genetic factors.},
   Language = {eng},
   Key = {fds216579}
}

@article{fds275651,
   Author = {Rezvani, AH and Overstreet, DH and Yang, Y and Clark,
             E},
   Title = {Attenuation of alcohol intake by extract of Hypericum
             perforatum (St. John's Wort) in two different strains of
             alcohol-preferring rats.},
   Journal = {Alcohol and Alcoholism (Oxford, Oxfordshire)},
   Volume = {34},
   Number = {5},
   Pages = {699-705},
   Year = {1999},
   Month = {September},
   ISSN = {0735-0414},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/10528812},
   Abstract = {Extract of the common plant Hypericum perforatum L. (St
             John's Wort, SJW) has been used successfully for the
             treatment of mild to moderate depression since ancient times
             and has recently been studied clinically. Depression and
             alcoholism have some neurochemical similarities, such as low
             brain serotonin activities. Thus, we hypothesized that SJW
             extract, which contains 0.22% hypericin and 4.05%
             hyperforin, also may be effective in suppressing alcohol
             intake. To test this hypothesis, the effects of SJW extract
             on voluntary alcohol intake were studied in two different
             genetic animal models of human alcoholism: fawn-hooded (FH)
             and high-alcohol drinking (HAD) rats. FH and HAD rats
             received a single oral administration (5 ml/kg) of either
             vehicle or one of the five doses (100, 200, 400, 600, and
             800 mg/kg) of SJW extract. The oral administration of SJW
             extract significantly (P < 0.0001) reduced alcohol intake in
             both FH and HAD rats. In a third study, FH rats did not
             develop tolerance to the suppressant effects of SJW on
             alcohol intake and preference following oral administration
             of (400 mg/kg) of the extract for 15 consecutive days. These
             promising findings suggest that SJW extract should be
             evaluated clinically as a potential therapeutic agent in the
             treatment of alcoholism.},
   Key = {fds275651}
}

@article{fds275652,
   Author = {Cowen, MS and Rezvani, AH and Jarrott, B and Lawrence,
             AJ},
   Title = {Ethanol consumption by Fawn-Hooded rats following
             abstinence: effect of naltrexone and changes in mu-opioid
             receptor density.},
   Journal = {Alcoholism, Clinical and Experimental Research},
   Volume = {23},
   Number = {6},
   Pages = {1008-1014},
   Year = {1999},
   Month = {June},
   ISSN = {0145-6008},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/10397284},
   Keywords = {Alcohol Drinking • Animals • Binding Sites •
             Central Nervous System Depressants •
             D-Ala(2),MePhe(4),Met(0)-ol-enkephalin • Ethanol •
             Male • Naltrexone • Narcotic Antagonists •
             Prosencephalon • Rats • Receptors, Opioid, mu
             • Temperance* • administration & dosage* •
             analysis • chemistry • drug effects • drug
             effects* • drug therapy* • pharmacology •
             pharmacology*},
   Abstract = {BACKGROUND: Relapse after abstinence can be modelled in rats
             using an alcohol deprivation effect (ADE) of enhanced
             ethanol consumption after a period of enforced abstinence
             from ethanol; however, not all rat strains display such an
             effect. We wanted to examine the effect of naltrexone on
             ethanol consumption by ethanol-preferring Fawn-Hooded (FH)
             rats using such a model. METHODS: FH rats were given
             continual free-choice access to a 5% ethanol solution or
             water (4 weeks) followed by 2 weeks of water alone. At the
             end of this abstinence period, osmotic minipumps were
             implanted subcutaneously to deliver saline (n = 4) or
             naltrexone (n = 4; 8.4 mg/kg/day for 4 weeks). After
             recovery from surgery, the rats were again given access to
             5% ethanol under the same free-choice conditions (4 weeks).
             A third group of age-matched controls drank only water
             during the behavioral trial. At the end of the behavioral
             trial, the rats were decapitated and an autoradiographic
             examination was made of micro-opioid receptor density
             through the forebrain using the ligand [125I]FK-33824.
             RESULTS: First, a period of enforced abstinence from ethanol
             consumption caused a significant (p < 0.05) and prolonged
             increase in ethanol preference (+18%) and decrease in water
             consumption (-53%), although the volume of ethanol consumed
             (ml/day) did not vary, indicating an atypical ADE in this
             rat strain. Second, naltrexone significantly (p < 0.05)
             decreased ethanol consumption by the FH rats in terms of
             absolute amount of ethanol consumed and preference for
             ethanol solution, but this effect of naltrexone diminished
             over time, concurrent with a robust and significant
             elevation in micro-opioid receptor density in all brain
             regions examined (p < 0.05). Finally, ethanol consumption
             alone also upregulated micro-opioid receptor density
             relative to nondrinking controls in a number of brain
             regions, which included the nucleus accumbens (+29%) and
             caudate-putamen (+15%,p < 0.05), but decreased micro-opioid
             receptor density in other regions including the substantia
             nigra pars reticulata, which was suggestive of an indirect
             effect on micro-opioid receptors. CONCLUSIONS: The data
             suggest that continual long-term naltrexone treatment may
             not be effective in the treatment of alcoholism, possibly
             because of the induced increase in micro-opioid receptor
             density.},
   Language = {eng},
   Doi = {10.1111/j.1530-0277.1999.tb04218.x},
   Key = {fds275652}
}

@article{fds275653,
   Author = {Overstreet, DH and Rezvani, AH and Parsian, A},
   Title = {Behavioural features of alcohol-preferring rats: focus on
             inbred strains.},
   Journal = {Alcohol and Alcoholism (Oxford, Oxfordshire)},
   Volume = {34},
   Number = {3},
   Pages = {378-385},
   Year = {1999},
   Month = {May},
   ISSN = {0735-0414},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/10414614},
   Abstract = {A recent study conducted a factor analysis on 18 behavioural
             measures obtained from four alcohol-preferring and five
             alcohol-non-preferring rat lines/strains. It was concluded
             that variables such as saccharin intake, ultrasonic
             vocalizations following an air puff, and defaecation in an
             open field were associated with voluntary and forced alcohol
             consumption. In contrast, measures such as time immobile in
             the forced swim test and time spent in the open arms of the
             elevated plus maze were not consistently associated with
             voluntary alcohol intake. The present study focuses on
             alcohol intake and related measures in four inbred strains
             of Fawn-Hooded (FH) rats that differ in voluntary alcohol
             intake and the ACI/N inbred rat strain, which voluntarily
             consumes very little alcohol. FH rats inbred by Jean Dodds
             (FH/Wjd) drank significantly more alcohol than FH rats
             inbred by Gordon Harrington (FH/Har) or selectively inbred
             by Abraham Provoost (FHH/Eur and FHL/EUR). In contrast, only
             the FH/Har strain was active in the forced swim test,
             suggesting that immobility and voluntary alcohol intake may
             be influenced by different genetic factors. The FH/Wjd rats
             were also much more immobile than the ACI/N rats in the
             forced swim test and drank almost 10 times as much alcohol
             voluntarily. Comparing the two parental lines with
             reciprocal F1 crosses revealed that alcohol consumption was
             influenced largely by additive genetic factors (F1 progeny
             had intermediate scores), whereas immobility was also
             influenced by dominance genetic factors (F progeny resembled
             the FH/Wjd parent). Preliminary analysis of 43 F2 progeny
             indicated that alcohol intake and immobility were not
             correlated. Thus, immobility in the forced swim test and
             high voluntary consumption of alcohol, two prominent
             features of the FH/Wjd rat strain which may be related to
             its serotonergic dysfunction, appear to be mediated by
             different genetic factors.},
   Key = {fds275653}
}

@article{fds275654,
   Author = {Tizabi, Y and Overstreet, DH and Rezvani, AH and Louis, VA and Clark, E and Janowsky, DS and Kling, MA},
   Title = {Antidepressant effects of nicotine in an animal model of
             depression.},
   Journal = {Psychopharmacology},
   Volume = {142},
   Number = {2},
   Pages = {193-199},
   Year = {1999},
   Month = {February},
   ISSN = {0033-3158},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/10102772},
   Keywords = {Alkaloids • Animals • Antidepressive Agents •
             Azocines • Binding Sites • Body Temperature •
             Bungarotoxins • Depression • Disease Models,
             Animal • Iodine Radioisotopes • Male • Motor
             Activity • Nicotine • Nicotinic Agonists •
             Quinolizines • Rats • Receptors, Nicotinic •
             Tritium • drug effects • drug therapy* •
             metabolism • pharmacology • therapeutic use •
             therapeutic use*},
   Abstract = {Epidemiological studies indicate a high incidence of
             cigarette smoking among depressed individuals. Moreover,
             individuals with a history of depression have a much harder
             time giving up smoking. It has been postulated that smoking
             may reflect an attempt at self-medication with nicotine by
             these individuals. Although some animal and human studies
             suggest that nicotine may act as an antidepressant, further
             verification of this hypothesis and involvement of nicotinic
             cholinergic system in depressive symptoms is required.
             Flinders Sensitive Line (FSL) rats have been proposed as an
             animal model of depression. These rats, selectively bred for
             their hyperresponsiveness to cholinergic stimulation, show
             an exaggerated immobility in the forced swim test compared
             to their control Flinders Resistant Line (FRL) rats. Acute
             or chronic (14 days) administration of nicotine (0.4 mg/kg
             s.c.) significantly improved the performance of the FSL but
             not the FRL rats in the swim test. The effects of nicotine
             on swim test were dissociable from its effects on locomotor
             activity. Moreover, the FSL rats had significantly higher
             [3H]cytisine binding (selective for the alpha4beta2
             nicotinic receptor subtype) but not [125I]alpha-bungarotoxin
             binding (selective for the alpha7 subtype) in the frontal
             cortex, striatum, midbrain and colliculi compared to FRL
             rats. These data strongly implicate the involvement of
             central nicotinic receptors in the depressive
             characteristics of the FSL rats, and suggest that nicotinic
             agonists may have therapeutic benefits in depressive
             disorders.},
   Language = {eng},
   Key = {fds275654}
}

@article{fds275649,
   Author = {Cowen, MS and Rezvani, A and Jarrott, B and Lawrence,
             AJ},
   Title = {Distribution of opioid peptide gene expression in the limbic
             system of Fawn-Hooded (alcohol-preferring) and Wistar-Kyoto
             (alcohol-non-preferring) rats},
   Journal = {Brain Research},
   Volume = {796},
   Number = {1-2},
   Pages = {323-326},
   Year = {1998},
   ISSN = {0006-8993},
   url = {http://dx.doi.org/10.1016/S0006-8993(98)00432-6},
   Abstract = {Preprodynorphin and preproenkephalin mRNA expression was
             examined in the CNS of two rat strains, the
             alcohol-preferring Fawn-Hooded (FH) and the
             alcohol-non-preferring Wistar-Kyoto (WKY), using in situ
             hybridisation histochemistry. Relative to the WKY, the FH
             showed significantly lower levels of preproenkephalin mRNA
             in the striatum and nucleus accumbens (-24% and - 17%
             respectively), but a higher level of preprodynorphin mRNA in
             the hippocampus (+33%). The depressed level of
             preproenkephalin mRNA in the nucleus accumbens may be
             implicated in alcohol-seeking behaviour.},
   Doi = {10.1016/S0006-8993(98)00432-6},
   Key = {fds275649}
}

@article{fds275643,
   Author = {Mason, GA and Rezvani, AH and Overstreet, DH and Hamedi, M and Walker,
             CH and Yang, Y and Garbutt, JC},
   Title = {Involvement of dopamine D2 receptors in the suppressive
             effect of the thyrotropin-releasing hormone analog TA-0910
             on alcohol intake in alcohol-preferring rats.},
   Journal = {Alcoholism, Clinical and Experimental Research},
   Volume = {21},
   Number = {9},
   Pages = {1623-1629},
   Year = {1997},
   Month = {December},
   ISSN = {0145-6008},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9438522},
   Keywords = {Alcohol Drinking • Animals • Behavior, Animal
             • Dose-Response Relationship, Drug • Drinking
             Behavior • Ethanol • Male • Nootropic Agents
             • Rats • Receptors, Dopamine D2 •
             Thyrotropin-Releasing Hormone • administration & dosage
             • analogs & derivatives* • drug effects •
             drug effects* • genetics* • pharmacology •
             pharmacology*},
   Abstract = {Pharmacological experiments were conducted to determine the
             neuronal mechanisms involved in the suppressive effects of
             the thyrotropin-releasing hormone analog TA-0910 on alcohol
             intake in alcohol-preferring (P) rats. We previously
             reported that single intraperitoneal injections of TA-0910
             dose-dependently reduced alcohol intake in P rats without
             altering fluid or total calorie intake; however, after
             several consecutive, once-daily injections, P rats developed
             tolerance to the suppressive effects of TA-0910 on alcohol
             intake and cross-tolerance to like effects of the dopamine
             D2 agonist bromocriptine, but not to like effects of the
             serotonin uptake inhibitor fluoxetine. In the present study,
             rats were injected with vehicle or different doses of the D2
             antagonist s(-)-eticlopride (0.01 to 0.05 mg/kg) or the D1
             antagonist R(+)-SCH23390 (0.1 to 0.5 mg/kg) and 20 min later
             with TA-0910 (0.75 mg/kg). Alcohol and water intakes were
             measured at 2, 4, 6, and 24 hr, and food was measured every
             24 hr. Both s(-)-eticlopride and R(+)-SCH23390 produced
             modest reductions in alcohol intake alone; however, only
             s(-)-eticlopride antagonized the suppressive effect of
             TA-0910 on alcohol intake. In related experiments, it was
             confirmed that the dopamine D3 agonist 7-hydroxy-N,N-di-n-propyl-2-aminotetralin
             reduced alcohol intake in P rats, and it was found that
             tolerance to this effect did not develop during or after
             seven consecutive once-daily injections. Furthermore, this
             effect of 7-hydroxy-N,N-di-n-propyl-2-aminotetralin was not
             diminished in rats made tolerant to the effect of TA-0910 on
             alcohol intake. These data, those of previous studies, and
             recent preliminary findings support involvement of dopamine
             D2, but not D1 or D3 receptors in mediating the suppressive
             effect of TA-0910 on alcohol intake of P
             rats.},
   Language = {eng},
   Key = {fds275643}
}

@article{fds275648,
   Author = {Chen, F and Rezvani, A and Jarrott, B and Lawrence,
             AJ},
   Title = {[3H]zolpidem binding in alcohol-preferring and
             non-preferring rat brain.},
   Journal = {Neuroscience Letters},
   Volume = {238},
   Number = {3},
   Pages = {103-106},
   Year = {1997},
   Month = {December},
   url = {http://dx.doi.org/10.1016/s0304-3940(97)00867-7},
   Abstract = {The present study has employed in vitro autoradiography to
             study the distribution and density of [3H]zolpidem binding
             sites, which are regarded as an index of ethanol-sensitive
             gamma-aminobutyric acid (GABA)A receptors, in the brains of
             alcohol-preferring Fawn-Hooded (FH) rats compared to
             non-alcohol preferring Wistar-Kyoto (WKY) rats. Binding of
             [3H]zolpidem showed a similar distribution profile in both
             rat strains examined and included cerebellum, globus
             pallidus, nucleus of the solitary tract and a number of
             midbrain/hindbrain nuclei. Densitometric quantitation of
             binding revealed that FH rats possessed a significantly
             higher density of [3H]zolpidem binding compared to WKY rats
             in cortical regions, substantia nigra pars reticulata and
             the ventral pallidum. These data indicate that FH rats may
             have an increased number of ethanol-sensitive GABA(A)
             receptors in regions intimately involved in reward
             processes, and may partially explain the alcohol-seeking
             nature of the FH rat.},
   Doi = {10.1016/s0304-3940(97)00867-7},
   Key = {fds275648}
}

@article{fds275640,
   Author = {Overstreet, DH and McArthur, RA and Rezvani, AH and Post,
             C},
   Title = {Selective inhibition of alcohol intake in diverse
             alcohol-preferring rat strains by the 5-HT2A antagonists
             amperozide and FG 5974.},
   Journal = {Alcoholism, Clinical and Experimental Research},
   Volume = {21},
   Number = {8},
   Pages = {1448-1454},
   Year = {1997},
   Month = {November},
   ISSN = {0145-6008},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9394117},
   Keywords = {Alcohol Drinking • Alcoholism • Animals •
             Consummatory Behavior • Dose-Response Relationship,
             Drug • Motivation* • Nicotinic Acids •
             Piperazines • Rats • Rats, Inbred Strains •
             Receptor, Serotonin, 5-HT2A • Receptors, Serotonin
             • Selection, Genetic • Serotonin Antagonists
             • drug effects • genetics* • pharmacology*
             • physiology • physiopathology},
   Abstract = {The present studies sought to elucidate the role of 5-HT2A
             receptor antagonists in suppressing alcohol intake by
             comparing the effects of amperozide and FG 5974 on alcohol,
             food, and water intake in strains of alcohol-preferring
             rats: P, Alko Alcohol (AA), and Fawn-Hooded (FH). Both
             amperozide and FG 5974 have 5-HT2A receptor antagonist
             properties, but FG 5974 also shows presynaptic 5-HT1A
             receptor agonist activity. After establishment of stable
             baselines for intake measures in a two-bottle continuous
             access paradigm, rats (n = 10) were injected with 1 of 5
             doses (0, 2.5, 5.0, and 10.0 mg/kg, sc) of amperozide or FG
             5974 at weekly intervals. Amperozide dose-dependently
             reduced alcohol intake, total fluid intake, and alcohol
             preference in all three strains under continuous access
             conditions, whereas FG 5974 was less effective. Food intake
             was also suppressed by amperozide at higher doses, whereas
             it was increased by FG 5974. Amperozide also
             dose-dependently reduced alcohol intake when it was
             available for only 1 hr/day, but FG 5974 tended to increase
             it. After oral administration, amperozide was also more
             effective than FG 5974 in reducing alcohol intake. Despite
             these differences in efficacy in suppressing alcohol intake,
             both compounds produced taste aversion to a novel saccharin
             solution. These complex findings suggest that biochemical
             properties other than 5-HT2A receptor antagonism (e.g.,
             5-HT1A receptor agonism) may be involved in the effects of
             amperozide and FG 5974 on alcohol intake and other
             consummatory behaviors.},
   Language = {eng},
   Key = {fds275640}
}

@article{fds275642,
   Author = {Knapp, DJ and Kampov-Polevoy, AB and Overstreet, DH and Breese, GR and Rezvani, AH},
   Title = {Ultrasonic vocalization behavior differs between lines of
             ethanol-preferring and nonpreferring rats.},
   Journal = {Alcoholism, Clinical and Experimental Research},
   Volume = {21},
   Number = {7},
   Pages = {1232-1240},
   Year = {1997},
   Month = {October},
   ISSN = {0145-6008},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9347084},
   Keywords = {Alcohol Drinking • Alcoholism • Animals •
             Arousal • Male • Motivation • Rats •
             Rats, Inbred Strains • Reaction Time • Species
             Specificity • Ultrasonics • Vocalization, Animal
             • genetics • genetics* • physiology*},
   Abstract = {To further understand the relationship between emotional
             state and alcohol intake in rats, the tendency to emit
             ultrasonic vocalizations in response to an aversive, but
             nonpainful, air puff stimulus was tested in several rat
             lines. Included in this group were Maudsley Reactive (MR)
             and Non-Reactive (MNR) rats, and several lines of rats with
             either high ethanol preference or a low ethanol preference:
             Preferring, (P), Alko-Alcohol (AA), and Fawn-Hooded (FH)
             animals; and Non-Preferring (NP), Alko-Non-Alcohol (ANA),
             and Flinders Resistant Line (FRL). MR rats emitted fewer
             ultrasonic vocalizations (USVs) and showed less preference
             for ethanol than did MNR animals. An overall analysis that
             included the P, NP, FH, FRL, AA, and ANA groups demonstrated
             a significant negative correlation between the total number
             of USVs emitted and ethanol consumption. NP, FRL, and
             especially ANA rats (low ethanol-preferring) emitted the
             most USVs--to an extent similar to that typically found for
             normal rats. The duration of vocalizing was higher only in
             the NP and the FRL rats the relative to their P and FH
             comparison groups, respectively. In the ethanol-preferring
             and nonpreferring lines, the numbers of USVs emitted
             correlated positively with the duration of vocalizing, but
             not with the latency to vocalize, which in turn did not
             correlate strongly with ethanol intake. The latency to
             vocalize did not correlate significantly with ethanol intake
             across all drinking lines or MR or MNR rats, but was found
             to be higher in FH and AA rats relative to their nondrinking
             comparison groups. These associations suggest that the
             relationship between emotional state and ethanol drinking is
             complex and cannot be attributed to a simple elevated state
             of anxiety or emotionality. Further examination of the
             central nervous system mechanisms mediating the difference
             in USVs between paired lines of ethanol-preferring and
             nonpreferring rats may identify neurochemical factors that
             predict ethanol preference.},
   Language = {eng},
   Doi = {10.1111/j.1530-0277.1997.tb04443.x},
   Key = {fds275642}
}

@article{fds275645,
   Author = {Rezvani, AH and Overstreet, DH and Yang, Y and Maisonneuve, IM and Bandarage, UK and Kuehne, ME and Glick, SD},
   Title = {Attenuation of alcohol consumption by a novel nontoxic
             ibogaine analogue (18-methoxycoronaridine) in
             alcohol-preferring rats.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {58},
   Number = {2},
   Pages = {615-619},
   Year = {1997},
   Month = {October},
   ISSN = {0091-3057},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9300627},
   Keywords = {Alcohol Drinking • Animals • Dose-Response
             Relationship, Drug • Ibogaine • Male • Rats
             • analogs & derivatives* • drug therapy* •
             pharmacology},
   Abstract = {We previously reported that single administration of
             ibogaine, an indol alkaloid with antiaddictive properties,
             dose dependently reduced alcohol intake in three strains of
             alcohol-preferring rats. The present study examined the
             effect of different doses of a newly developed nontoxic
             ibogaine analogue, 18-methoxycoronaridine (18-MC), on
             alcohol intake. Selectively bred alcohol-preferring rats
             received a single intraperitoneal injection of vehicle or 5,
             20 and 40 mg/kg of 18-MC at 9:30 AM, and their consumption
             of alcohol, water and food was measured for 24 h. Our
             results demonstrate that a single injection of 18-MC
             significantly and dose dependently attenuated alcohol
             consumption and preference and commensurately increased
             water intake. Only the highest dose of 18-MC significantly
             decreased food intake. Although the true mechanism of action
             of 18-MC in suppressing alcohol intake is not yet fully
             understood, it may, like ibogaine, exert its attenuating
             effects on alcohol consumption by modulating
             neurotransmitters believed to be involved in the regulation
             of alcohol intake.},
   Language = {eng},
   Doi = {10.1016/s0091-3057(97)10003-x},
   Key = {fds275645}
}

@article{fds275647,
   Author = {Kampov-Polevoy, AB and Rezvani, AH},
   Title = {Fluoxetine reduces saccharin-induced elevation of fluid
             intake in alcohol-preferring Fawn-Hooded
             rats.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {58},
   Number = {1},
   Pages = {51-54},
   Year = {1997},
   Month = {September},
   ISSN = {0091-3057},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9264069},
   Keywords = {Alcohol Drinking • Animals • Antidepressive
             Agents, Second-Generation • Dose-Response Relationship,
             Drug • Drinking • Fluoxetine • Male •
             Rats • Saccharin • drug effects* • genetics
             • pharmacology* • psychology*},
   Abstract = {Previous work has established that saccharin and alcohol
             intakes are highly correlated in a variety of rat strains.
             In addition, it has been shown that alcohol-preferring rats
             consume saccharin beyond the limit of their normal daily
             fluid intake (DFI). It has been hypothesized that
             alcohol-preferring rats have impaired control over
             consumption of reinforcing substances, which may be related
             to a deficiency of brain serotonin. In the present study, we
             examined the effect of the serotonin reuptake inhibitor
             fluoxetine (2.5, 5.0, 10.0 mg/kg, IP, twice a day) on
             saccharin intake in alcohol-preferring Fawn-Hooded (FH)
             rats. It was confirmed that alcohol preferring FH rats
             almost triple their DFI when saccharin/water choice was
             introduced. Treatment with fluoxetine resulted in a
             dose-dependent decrease in saccharin intake to, but not
             below, the normal level of their DFI. No significant effects
             of fluoxetine on water intake were observed. Despite a
             significant (up to 69%) decrease in saccharin intake, only a
             minimal reduction (< 4%) in saccharin preference occurred.
             We conclude that fluoxetine reduces the exessive elevation
             of fluid intake observed at the presence of the palatable
             saccharin solution in Fawn-Hooded rats. These findings may
             provide more evidence for the involvement of the
             serotonergic system in the brain in exessive drinking of
             rewarding substances.},
   Language = {eng},
   Key = {fds275647}
}

@article{fds275672,
   Author = {Overstreet, DH and Halikas, JA and Seredenin, SB and Kampov-Polevoy,
             AB and Viglinskaya, IV and Kashevskaya, O and Badishtov, BA and Knapp,
             DJ and Mormede, P and Kiianmaa, K and Li, TK and Rezvani,
             AH},
   Title = {Behavioral similarities and differences among
             alcohol-preferring and -nonpreferring rats: confirmation by
             factor analysis and extension to additional
             groups.},
   Journal = {Alcoholism, Clinical and Experimental Research},
   Volume = {21},
   Number = {5},
   Pages = {840-848},
   Year = {1997},
   Month = {August},
   ISSN = {0145-6008},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9267533},
   Keywords = {Alcohol Drinking • Animals • Arousal •
             Behavior, Animal • Emotions • Factor Analysis,
             Statistical • Male • Motivation* • Motor
             Activity • Rats • Rats, Inbred Strains •
             Species Specificity • Taste • genetics •
             genetics* • physiology • physiology*},
   Abstract = {Thirteen behavioral variables from six tasks were measured
             in alcohol-preferring (AA, FH, and P) and -nonpreferring
             (ANA, FRL, and NP) rat lines/strains and subjected to Factor
             Analysis. Four Independent factors accounted for > 90% of
             the variance. Defecation in the open field and ultrasonic
             vocalizations after an air puff were negatively correlated
             with alcohol intake and preference, whereas the increase in
             daily fluid intake in the presence of saccharin was
             positively correlated. Other factors could be labeled
             Activity, Emotionality, and immobility Factors, and each was
             independent of the Alcohol Factor. When an additional
             alcohol-preferring rat line (HAD) and two additional
             nonpreferring groups (LAD and ACI) were tested, they were
             found to differ on most behaviors that were associated with
             alcohol intake and preference in the Factor Analysis;
             vocalizations and saccharin-induced increase in fluid
             intake, but not defection. A new Factor Analysis was then
             performed incorporating these three new groups and including
             five new behavioral measures. The following measures had
             high loadings on the Alcohol Factor: alcohol intake under
             choice conditions; alcohol preference; forced alcohol
             intake; alcohol acceptance (forced alcohol intake/basal
             water intake x 100); ultrasonic vocalization; saccharin
             intake; saccharin-induced increase in daily fluid intake;
             defecation in the open field test; and immobility in a
             modified forced swim test. These findings indicate that
             there are indeed certain behavioral characteristics that are
             common among alcohol-preferring rat lines/strains, but there
             are also substantial group differences on other behavioral
             measures. For those behavioral measures reflecting
             emotionality (defecation and ultrasonic vocalization) that
             loaded highly on the Alcohol Factor, the alcohol-preferring
             rats had lower scores.},
   Language = {eng},
   Doi = {10.1111/j.1530-0277.1997.tb03847.x},
   Key = {fds275672}
}

@article{fds275644,
   Author = {Rezvani, AH and Garbutt, JC and Overstreet, DH and Li, L and Walker, CH and Yang, Y and Mason, GA},
   Title = {Thyrotropin releasing hormone analog TA-0910 suppresses
             alcohol intake in alcohol drinking African green
             monkeys.},
   Journal = {Alcoholism, Clinical and Experimental Research},
   Volume = {21},
   Number = {2},
   Pages = {261-266},
   Year = {1997},
   Month = {April},
   ISSN = {0145-6008},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/9113262},
   Keywords = {Alcohol Drinking • Animals • Cercopithecus
             aethiops • Drinking • Male • Motivation
             • Neurotransmitter Agents • Nootropic Agents
             • Rats • Saccharin • Species Specificity
             • Taste • Thyrotropin-Releasing Hormone •
             administration & dosage • analogs & derivatives* •
             drug effects • pharmacology • pharmacology* •
             physiology • physiopathology*},
   Abstract = {In previous studies, we found that single injections of the
             thyrotropin-releasing hormone analog TA-0910
             dose-dependently reduced alcohol intake and preference in
             alcohol-preferring (P) and Fawn-Hooded (FH) rats over a
             24-hr period of continuous access to alcohol and water.
             However, several consecutive daily injections of TA-0910
             resulted in the development of tolerance to these effects.
             In the present study, we found that in a 5-hr limited-access
             schedule in which monkeys could select an aqueous alcohol
             solution (7.5% v/v) or tap water, single doses of TA-0910
             (0.0625, 0.125, 0.25, 0.5, and 0.75 mg/kg), similar to those
             found effective in P and FH rats, reduced consumption of
             alcohol. In this protocol, tolerance to the attenuating
             effects of TA-0910 on alcohol intake was not evident after
             five consecutive once-daily doses of 0.5 mg/kg. Furthermore,
             it was shown that a single dose of 0.75 mg/kg TA-0910 did
             not significantly influence 24-hr water intake when water
             was the only available fluid, but did reduce the intake of a
             preferred solution of saccharin. These findings suggest that
             activation of brain thyrotropin-releasing hormone systems
             reduces alcohol intake in primates and that tolerance to
             this effect is not evident within 5 days under a limited
             access schedule.},
   Language = {eng},
   Key = {fds275644}
}

@article{fds275646,
   Author = {Chen, F and Rezvani, A and Jarrott, B and Lawrence,
             AJ},
   Title = {Distribution of GABA(A) receptors in the limbic system of
             alcohol-preferring and non-preferring rats: In situ
             hybridisation histochemistry and receptor
             autoradiography},
   Journal = {Neurochemistry International},
   Volume = {32},
   Number = {2},
   Pages = {143-151},
   Year = {1997},
   url = {http://dx.doi.org/10.1016/S0197-0186(97)00069-7},
   Abstract = {The present study has employed quantitative receptor
             autoradiography and in situ hybridisation histochemistry to
             compare the expression of the mRNA encoding the α1 and α2
             subunits of the GABA(A) receptor and the binding density of
             mature GABA(A) receptors in the limbic system of
             alcohol-preferring Fawn-Hooded rats (FH) with Wistar-Kyoto
             rats (WKY). Quantifiable levels of mRNA encoding the α1
             subunit were found in cortical regions, ventral pallidum,
             substantia nigra, horizontal limb of the diagonal band and
             the hippocampus of both rat strains. Interestingly,
             expression of the α1 subunit mRNA was decreased by
             approximately 30% in the hippocampus of FH compared to WKY
             rats. Following a 28-day period with free access to 10%
             ethanol, expression of the α1 subunit transcript, was
             significantly increased in the piriform cortex and
             horizontal limb of the diagonal band, unaltered in the
             hippocampus but decreased in the substantia nigra of FH
             rats. Quantifiable levels of mRNA encoding the α2 subunit
             were found in nucleus accumbens, amygdala, cortical regions,
             lateral septal nucleus, hippocampus, medial habenula and
             ventral pallidum of both strains. Expression of the α2
             subunit mRNA was decreased by approximately 35% in both the
             hippocampus and occipital cortex of FH compared to WKY rats.
             However, consumption of 10% ethanol in FH rats had no impact
             upon expression of the mRNA encoding the α2 subunit in any
             region examined. Mature GABA(A) receptors were studied by
             autoradiography utilising the antagonist radioligand
             [3H]SR95531 and the agonist radioligand [3H]muscimol.
             Topographic binding throughout the limbic system of both
             strains was observed for both radioligands. Specifically,
             [3H]SR95531 binding was higher in the occipital cortex,
             hippocampus, lateral septal nucleus, superior colliculus and
             ventral pallidum of the FH rats compared to WKY rats;
             however, in the nucleus accumbens [3H]SR95531 binding was
             lower in FH compared to WKY. Ethanol consumption had no
             measurable effect on the binding of [3H]SR95531 in FH rats.
             In the case of [3H]muscimol, binding was higher in the
             cortex, lateral septum and ventral pallidum of FH compared
             to WKY. Furthermore, ethanol consumption resulted in a
             25-30% increase in [3H]muscimol binding in the lateral
             septum and striatum of FH rats. These data provide evidence
             for differential expression of GABA(A) receptor sunbunits in
             FH and WKY rats, and additionally indicate anatomically
             defined variations in GABA(A) receptor binding between the
             two rat strains.},
   Doi = {10.1016/S0197-0186(97)00069-7},
   Key = {fds275646}
}

@article{fds275636,
   Author = {Overstreet, DH and Rezvani, AH},
   Title = {Behavioral differences between two inbred strains of
             Fawn-Hooded rat: a model of serotonin dysfunction.},
   Journal = {Psychopharmacology},
   Volume = {128},
   Number = {3},
   Pages = {328-330},
   Year = {1996},
   Month = {December},
   ISSN = {0033-3158},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8972553},
   Keywords = {Alcohol Drinking • Animals • Avoidance Learning
             • Behavior, Animal • Feeding Behavior* • Rats
             • Rats, Inbred Strains • Rats, Sprague-Dawley
             • Receptors, Serotonin • Saccharin • Self
             Administration • Species Specificity • Swimming
             • administration & dosage • genetics •
             physiology • physiology*},
   Abstract = {The Fawn-Hooded rat (FH) strain has attracted the attention
             of some psychopharmacologists because of reports of its
             exaggerated immobility in the swim test, hypercortisolemia,
             excessive voluntary intake of alcohol, platelet and central
             serotonin abnormalities and subsensitivity to serotonergic
             agonists. However, there appears to be some controversy over
             several behavioral and physiological characteristics of
             these rats. The present paper proposes that the lack of
             reproducible findings can be traced to there being several
             distinct inbred strains of FH rats. Of the two compared in
             this communication, the FH/Wjd strain is more immobile in
             the forced swim test, spends more time in the open arms of
             the elevated plus maze, and drinks more saccharin and
             alcohol voluntarily than the FH/Har (Iowa Reactive) strain.
             Future workers are cautioned to report the source of their
             FH rats.},
   Language = {eng},
   Key = {fds275636}
}

@article{fds275637,
   Author = {Mason, GA and Rezvani, AH and Overstreet, DH and Garbutt,
             JC},
   Title = {Thyrotropin-releasing hormone analog TA-0910 reduces
             voluntary alcohol intake of P rats subchronically in a
             limited scheduled access paradigm.},
   Journal = {Alcoholism, Clinical and Experimental Research},
   Volume = {20},
   Number = {6},
   Pages = {1000-1003},
   Year = {1996},
   Month = {September},
   ISSN = {0145-6008},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8892518},
   Keywords = {Alcohol Drinking • Animals • Dose-Response
             Relationship, Drug • Injections, Intraperitoneal •
             Male • Motivation* • Nootropic Agents • Rats
             • Rats, Inbred Strains • Reinforcement Schedule
             • Thyrotropin-Releasing Hormone • analogs &
             derivatives* • pharmacology • pharmacology* •
             psychology*},
   Abstract = {We previously reported that single intraperitoneal
             injections of the thyrotropin-releasing hormone analog
             TA-0910 dose-dependently reduce alcohol intake in
             alcohol-preferring (P) rats in a free-choice continuous
             access protocol. We later showed, using the same protocol,
             that a transient tolerance develops to this effect after
             several consecutive, once-daily injections. In the present
             study, P rats that had been accustomed to continuous access
             to alcohol were acclimated to a limited scheduled access
             protocol in which alcohol was available only between 10 and
             11 AM. This resulted in an elevated rate of alcohol intake.
             Rats were then injected once daily with TA-0910 (0.75 mg/kg)
             or an equal volume of a saline vehicle at 9:45 AM for 12
             consecutive days. After 11 days of scheduled access, rats
             were allowed continuous access to alcohol. Intake of alcohol
             and water was measured each day at 11:00 AM. Compared with
             vehicle, TA-0910 reduced alcohol intake on the 11 days of
             scheduled access and during the first hour of day 12 when
             continuous access was restored, but did not reduce total (24
             hr) alcohol intake on day 12. Data from this experiment show
             that TA-0910 reduces alcohol intake over a long period of
             time in a limited scheduled access protocol.},
   Language = {eng},
   Key = {fds275637}
}

@article{fds275638,
   Author = {Overstreet, DH and Lee, YW and Rezvani, AH and Pei, YH and Criswell, HE and Janowsky, DS},
   Title = {Suppression of alcohol intake after administration of the
             Chinese herbal medicine, NPI-028, and its
             derivatives.},
   Journal = {Alcoholism, Clinical and Experimental Research},
   Volume = {20},
   Number = {2},
   Pages = {221-227},
   Year = {1996},
   Month = {April},
   ISSN = {0145-6008},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8730211},
   Keywords = {Alcohol Deterrents • Alcohol Drinking • Animals
             • Dose-Response Relationship, Drug • Drugs,
             Chinese Herbal • Ethanol • Injections,
             Intraperitoneal • Isoflavones • Rats • Rats,
             Inbred Strains • Structure-Activity Relationship •
             pharmacokinetics • pharmacology • pharmacology*
             • prevention & control*},
   Abstract = {The Chinese herbal medicine, NPI-028, has been used for
             centuries in China to counteract alcohol intoxication. The
             present study used a number of different experimental
             conditions to determine whether NPI-028 and its derivatives
             might selectively influence alcohol intake in rodents that
             naturally exhibit high alcohol intakes. It was determined
             that intraperitoneal (i.p.) injections of NPI-028 (0.5,
             0.75, and 1.0 g/kg) suppressed alcohol intake by up to 30%
             in both alcohol-preferring P and Fawn-Hooded (FH) rats
             during a continuous access schedule. These injections did
             not significantly affect food or water intakes, nor did the
             highest dose of NPI-028 (1 g/kg) alter blood ethanol levels
             after an i.p. injection of 2.5 g/kg of ethanol. In P rats,
             it was found that NPI-028 was orally active with the dose of
             1.5 g/kg having a greater effect on ethanol intake than the
             1.0 g/kg dose; once again, food and water intakes were not
             significantly altered. In FH rats maintained on a limited
             access schedule (1 hr/day), alcohol intake was completely
             abolished by 1.5 g/kg of NPI-028. Chronic i.p.
             administration of NPI-028 (0.75 g/kg) for four consecutive
             days in FH rats maintained on a continuous access schedule
             did not lead to any diminution of its alcohol-suppressant
             effects. Thus, NPI-028 has significant effects on alcohol
             intake without much effect on water and food intake, and
             tolerance does not readily develop to these effects. The
             i.p. administration of a partially purified extract
             (NPI-031) of NPI-028, obtained by countercurrent
             chromatography, also dose-dependently suppressed ethanol
             intake in FH rats, but the highest dose 200 mg/kg) also
             significantly decreased food intake. Finally, the i.p.
             administration of puerarin (NPI-31G), an isoflavone isolated
             from NPI-031 by countercurrent chromatography, significantly
             reduced ethanol intake in FH rats without affecting food or
             water intake. Therefore, NPI-028 and one of its pure
             components, NPI-031G, selectively reduced ethanol intake in
             alcohol-preferring rats.},
   Language = {eng},
   Doi = {10.1111/j.1530-0277.1996.tb01633.x},
   Key = {fds275638}
}

@article{fds275639,
   Author = {Kampov-Polevoy, AB and Kasheffskaya, OP and Overstreet, DH and Rezvani, AH and Viglinskaya, IV and Badistov, BA and Seredenin, SB and Halikas, JA and Sinclair, JD},
   Title = {Pain sensitivity and saccharin intake in alcohol-preferring
             and -nonpreferring rat strains.},
   Journal = {Physiology & Behavior},
   Volume = {59},
   Number = {4-5},
   Pages = {683-688},
   Year = {1996},
   Month = {April},
   ISSN = {0031-9384},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8778852},
   Keywords = {Alcohol Drinking • Animals • Pain • Pain
             Measurement • Rats • Rats, Inbred Strains •
             Reaction Time • Saccharin • Species Specificity
             • Sweetening Agents • Taste • drug effects
             • drug effects* • drug therapy • genetics
             • pharmacology* • physiology •
             psychology*},
   Abstract = {The experiments were designed to study the association
             between consumption of palatable 0.1% (w/v) saccharin
             solution, voluntary drinking of 10% (v/v) ethanol solution,
             and pain sensitivity measured with the hot plate test. Rat
             lines that were genetically selected for high alcohol
             consumption (P and AA rats), alcohol-preferring Fawn Hooded
             (FH) rats and their F2[FH x FRL] hybrids, and the Maudsley
             Nonreactive strain (MNRA) had a high propensity to consume
             saccharin that resulted in a significant (almost twofold; p
             < 0.05) increase in their daily fluid intake when saccharin
             was available. These strains also had lower pain thresholds
             in the hot plate test than did their parallel strains [NP,
             ANA, Maudsley Reactive (MR)]. Most alcohol-nonpreferring
             strains [NP, ANA, and Flinders Resistant Line (FRL)] had
             preference ratios for saccharin about as high as those of
             the alcohol-preferring rats but, unlike the high alcohol
             drinkers, they did not increase their total fluid intake
             when saccharin was available. The mean saccharin intakes of
             the lines were strongly correlated with their alcohol
             drinking during the first 5 days, whereas their latencies on
             the hot plate were inversely related to their change in
             alcohol drinking with experience. The results are consistent
             with an endogenous opioid mechanism being involved in
             alcohol drinking.},
   Language = {eng},
   Key = {fds275639}
}

@article{fds275641,
   Author = {Pucilowski, O and Rezvani, AH and Overstreet, DH},
   Title = {Role of taste aversion in calcium channel inhibitor-induced
             suppression of saccharin and alcohol drinking in
             rats.},
   Journal = {Physiology & Behavior},
   Volume = {59},
   Number = {2},
   Pages = {319-324},
   Year = {1996},
   Month = {February},
   ISSN = {0031-9384},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8838612},
   Keywords = {Alcohol Drinking • Animals • Avoidance Learning
             • Calcium Channel Blockers • Conditioning,
             Classical • Diltiazem • Dose-Response
             Relationship, Drug • Drinking • Isradipine •
             Male • Nicardipine • Rats • Rats,
             Sprague-Dawley • Saccharin* • Taste • drug
             effects* • pharmacology • pharmacology* •
             physiopathology* • psychology},
   Abstract = {L-type calcium (Ca2+) channel inhibitors suppress drinking
             of highly preferred solutions of simple carbohydrates,
             saccharin, or alcohol. The present study was designed to
             examine whether this decrease in drinking behavior can be
             explained by the development of consummatory aversion. In
             the first experiment, the propensity of Ca2+ channel
             inhibitors to induce conditioned taste aversion (CTA) to
             0.1% saccharin was examined using two saccharin/drug
             injection pairings in saccharin-naive rats. We compared
             three chemically different drugs: diltiazem, isradipine, and
             nicardipine. A dose-dependent CTA was observed after both
             conditioning sessions for all three drugs tested.
             Interestingly, the lowest dose of nicardipine (i.e., 1.25
             mumol/kg), significantly increased saccharin intake. A
             nonsignificant trend to increase saccharin intake was also
             observed with the lowest dose of isradipine. We then
             examined whether nicardipine could similarly induce CTA to a
             novel taste of alcohol (6%, v/v). The drug failed to produce
             a significant effect. In the third experiment, we found that
             nicardipine did not induce CTA (or preference) if the
             saccharin taste was familar to rats. In the final
             experiment, the interaction of nicardipine (1.25 and 2.5
             mumol/kg) with the ethanol (1.5 g/kg)-induced CTA to
             saccharin was investigated. The higher dose of nicardipine
             potentiated the aversive effect of ethanol in the test.
             Overall, the present results suggest that CTA does not play
             a major role in Ca2+ channel inhibitor-induced suppression
             of drinking behavior.},
   Language = {eng},
   Key = {fds275641}
}

@article{fds275756,
   Author = {Overstreet, DH and Rezvani, AH and Knapp, DJ and Crews, FT and Janowsky,
             DS},
   Title = {Further selection of rat lines differing in 5-HT-1A receptor
             sensitivity: behavioral and functional correlates.},
   Journal = {Psychiatric Genetics},
   Volume = {6},
   Number = {3},
   Pages = {107-117},
   Year = {1996},
   ISSN = {0955-8829},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8902886},
   Keywords = {8-Hydroxy-2-(di-n-propylamino)tetralin • Animals •
             Body Temperature • Crosses, Genetic • Ethanol
             • Female • Food Preferences • Male •
             Maze Learning* • Motor Activity* • Pindolol •
             Rats • Rats, Inbred Strains • Receptors, Serotonin
             • Receptors, Serotonin, 5-HT1 • Ritanserin •
             Saccharin • Selection, Genetic • Serotonin
             Antagonists • Serotonin Receptor Agonists • Taste
             • drug effects • genetics* • metabolism
             • pharmacology • pharmacology* •
             physiology},
   Abstract = {It was previously reported that selection for differences in
             the hypothermic effects to the selective 5-HT-1A agonist,
             8-OH-DPAT, occurred rapidly, with very substantial
             differences present by the fourth generation. The present
             communication summarizes the findings from the next five
             generations of selection and from behavioral and other
             functional studies on these rats. The rats which were more
             sensitive to 8-OH-DPAT (High DPAT Sensitive-HDS) exhibited
             decreases in temperature of 4 degrees C or more and the
             distribution did not overlap with that of the rats which
             were less sensitive to 8-OH-DPAT (Low DPAT Sensitive-LDS)
             which exhibited decreases in temperature of 1.5 degrees C or
             less. The randomly bred control group (Random DPAT
             Sensitive-RDS) exhibited intermediate temperature decreases
             (means of 1.6-1.8 degrees C), with time overlap with the
             distributions of the selected groups. Pretreatment with
             pindolol, a 5-HT-1A antagonist, reduced the hypothermic
             response to 8-OH-DPAT, but pretreatment with ritanserin, a
             5-HT-7 and 5-HT-2A/C antagonist, had no effect, confirming
             that the hypothermic response to 8-OH-DPAT is mediated
             predominantly by 5-HT-1A receptors. The HDS rats were less
             mobile in a forced swim test and drank more saccharin
             solution in a two-bottle choice paradigm than the LDS or RDS
             rats over several generations. In contrast, there were no
             consistent differences among the groups for open field
             activity or performance in an elevated plus maze. There were
             no differences among the groups for voluntary alcohol
             intake, but the HDS rats exhibited greater suppression of
             alcohol and saccharin intake after injection of 8-OH-DPAT
             (0.125 mg kg-1). The HDS rats were also found to have a
             higher number of 5-HT-1A binding sites in cortical regions
             than the LDS or RDS rats, but there were no 5-HT-1A binding
             site differences in the raphe nuclei. These findings clearly
             show that consistent behavioral differences do occur in the
             8-OH-DPAT-selected lines of rats, but only for behaviors
             related to possible depression or reward, not anxiety. The
             pattern of binding results suggests that these behavioral
             correlates of 8-OH-DPAT selection may be related to changes
             in cortical 5-HT-1A receptors rather than raphe
             autoreceptors.},
   Language = {eng},
   Key = {fds275756}
}

@article{fds275634,
   Author = {Rezvani, AH and Overstreet, DH and Lee, YW},
   Title = {Attenuation of alcohol intake by ibogaine in three strains
             of alcohol-preferring rats.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {52},
   Number = {3},
   Pages = {615-620},
   Year = {1995},
   Month = {November},
   ISSN = {0091-3057},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8545483},
   Keywords = {Alcohol Deterrents • Alcohol Drinking • Animals
             • Dose-Response Relationship, Drug • Drinking
             Behavior • Eating • Ethanol • Ibogaine •
             Male • Rats • blood • drug effects •
             genetics • pharmacology* • psychology*},
   Abstract = {Alcohol-preferring (P), Fawn-Hooded (FH) and
             alcohol-accepting (AA) rats were injected intraperitoneally
             (IP) or subcutaneously (SC) with different doses (10, 30,
             and 60 mg/kg) of Ibogaine or vehicle. In a separate
             experiment, FH rats were administered intragastrically (IG)
             with either 60 mg/kg of Ibogaine or vehicle for 5 days. In
             addition, the effects of Ibogaine on blood alcohol
             concentrations were measured. Our data show that, contrary
             to the SC administration of Ibogaine, IP administration of
             the agent significantly and dose-dependently reduced alcohol
             intake in these rats. Subchronic IG administration of 60
             mg/kg of Ibogaine into FH rats significantly reduced alcohol
             intake without the development of tolerance or a significant
             effect on food or water intake. A single IP injection of 60
             mg/kg Ibogaine into FH rats did not affect the blood alcohol
             levels. These results show that Ibogaine when injected IP or
             IG, but not SC, can significantly reduce alcohol intake
             without an effect on blood alcohol concentrations or food
             intake. These findings may suggest the involvement of
             Ibogaine's metabolite(s) in reducing alcohol intake.
             Although the neuronal mechanism(s) of action of Ibogaine on
             the regulation of alcohol intake is not fully understood, it
             is speculated that Ibogaine or its metabolite(s) exerts its
             attenuating effect on alcohol intake by modulating
             neurotransmitters/neuromodulators proposed to be involved in
             regulation of alcohol consumption.},
   Language = {eng},
   Doi = {10.1016/0091-3057(95)00152-m},
   Key = {fds275634}
}

@article{fds275633,
   Author = {Kampov-Polevoy, AB and Overstreet, DH and Rezvani, AH and Janowsky,
             DS},
   Title = {Suppression of ethanol intake in alcohol-preferring rats by
             prior voluntary saccharin consumption.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {52},
   Number = {1},
   Pages = {59-64},
   Year = {1995},
   Month = {September},
   ISSN = {0091-3057},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7501679},
   Keywords = {Alcohol Deterrents • Alcohol Drinking • Animals
             • Depression, Chemical • Drinking • Eating
             • Male • Rats • Saccharin • drug effects
             • genetics • pharmacology* •
             psychology*},
   Abstract = {In a situation offering a free choice between 0.1% saccharin
             solution and tap water, Fawn Hooded (FH) rats consumed 363.0
             +/- 33.5 ml/kg/day of saccharin solution. Subsequently those
             animals drank 3.0 +/- 0.4 g/kg of ethanol in a free choice
             between water and 10% ethanol solution. Control FH rats that
             did not have access to saccharin consumed 5.0 +/- 0.5
             between groups was significant: p = 0.006). When control
             rats were exposed to the choice between 10% ethanol solution
             and 0.1% saccharin solution for 4 days they consumed 383.7
             +/- 27.5 ml/kg/day of saccharin solution and their ethanol
             intake dropped to 1.2 +/- 0.3 g/kg/day. When these rats were
             returned back to alcohol/water choice and exposure to
             saccharin was discontinued, their alcohol intake was still
             reduced (3.7 +/- 0.3 g/kg/day for at least 10 consecutive
             days). Exposure of alcohol-experienced alcohol-preferring P
             rats with high (6.8 +/- 0.5 g/kg/day) and stable alcohol
             intake to saccharin/water choice for 4 days also resulted in
             a significant attenuation of their ethanol intake for at
             least 6 days following saccharin cessation. Thus, voluntary
             consumption of saccharin can suppress subsequent alcohol
             intake in both alcohol-naive and alcohol-experienced
             rats.},
   Language = {eng},
   Key = {fds275633}
}

@article{fds275635,
   Author = {Overstreet, DH and Pucilowski, O and Rezvani, AH and Janowsky,
             DS},
   Title = {Administration of antidepressants, diazepam and psychomotor
             stimulants further confirms the utility of Flinders
             Sensitive Line rats as an animal model of
             depression.},
   Journal = {Psychopharmacology},
   Volume = {121},
   Number = {1},
   Pages = {27-37},
   Year = {1995},
   Month = {September},
   ISSN = {0033-3158},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8539339},
   Keywords = {Animals • Antidepressive Agents • Depression
             • Diazepam • Disease Models, Animal* • Motor
             Activity • Rats • drug effects • drug
             therapy* • pharmacology*},
   Abstract = {Flinders Sensitive Line (FSL) rats have been proposed as an
             animal model of depression because they resemble depressed
             humans in that they have elevated REM sleep, reduced
             activity, and increased immobility and anhedonia after
             exposure to stressors. The present paper reviews experiments
             on the drug treatment of FSL and control Flinders Resistant
             Line (FRL) rats related to their utility as an animal model
             of depression, and presents new information. FSL rats
             exhibited exaggerated immobility in the forced swim test
             which is counteracted by the tricyclic antidepressants
             imipramine and desipramine and the serotonin reuptake
             blocker sertraline; the low immobility exhibited by the FRL
             rats is generally unaffected by these compounds. In contrast
             to these "therapeutic" effects of well recognized
             antidepressants, lithium and bright light treatment did not
             alter the exaggerated immobility of FSL rats. Novel data
             indicated that neither FSL nor FRL rats exhibited
             alterations in swim test immobility following chronic
             administration of the psychomotor stimulant amphetamine (2
             mg/kg) and the anticholinergic scopolamine (2 mg/kg), which
             typically reduce immobility after acute administration.
             However, it was found that the calcium channel blockers
             verapamil (5 and 15 mg/kg) and nicardipine (10 mg/kg) did
             reduce the exaggerated immobility in FSL rats following
             chronic administration, suggesting that these compounds need
             to be evaluated further in humans. Previous studies have
             indicated no differences between FSL and FRL rats evaluated
             in the elevated plus maze, either at baseline or after the
             administration of diazepam, suggesting that the FSL rat may
             not differ from controls in anxiety-related behavior.
             Another recently published study showed that the FSL rat
             also did not differ from normal Sprague-Dawley rats in
             startle tests, indicating that the FSL rats do not exhibit
             behaviors shown in animal models of schizophrenia. These
             findings confirm the utility of FSL rats as an animal model
             of depression because the FSL rats do not appear to exhibit
             behaviors analogous to anxiety or schizophrenia and because
             they respond "therapeutically" to antidepressants and not
             psychomotor stimulants.},
   Language = {eng},
   Key = {fds275635}
}

@article{fds275632,
   Author = {Kampov-Polevoy, AB and Overstreet, DH and Rezvani, AH and Janowsky,
             DS},
   Title = {Saccharin-induced increase in daily fluid intake as a
             predictor of voluntary alcohol intake in alcohol-preferring
             rats.},
   Journal = {Physiology & Behavior},
   Volume = {57},
   Number = {4},
   Pages = {791-795},
   Year = {1995},
   Month = {April},
   ISSN = {0031-9384},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7777619},
   Keywords = {Alcohol Drinking • Animals • Drinking • Male
             • Rats • Rats, Inbred Strains • Saccharin
             • Species Specificity • drug effects* •
             genetics • pharmacology* • psychology*},
   Abstract = {This study examined the relationship between saccharin
             intake and ethanol consumption in alcohol preferring (P)
             rats and Fawn Hooded (FH) rats before and after exposure to
             forced ethanol (10%, v/v) solution. Both groups exhibited
             large increases (> 2X) in daily fluid intake (DFI) when
             saccharin (0.1%, w/v) was present and exhibited moderate
             levels of ethanol intake. Only the P rats significantly
             increased their ethanol consumption after exposure to
             ethanol as the sole drinking fluid. Correlational analyses
             revealed that the absolute intakes of saccharin and ethanol
             were not significantly correlated in either group, but the
             increase in DFI in the presence of saccharin was highly
             correlated with ethanol intake after forced ethanol exposure
             (r > +0.8; p < 0.05). Similarly, when correlations were
             conducted for these variables over both the P and FH groups,
             the correlation between increase in DFI in the presence of
             saccharin and alcohol intake was significantly higher than
             that between saccharin and alcohol intakes. Reexamination of
             previous data from 6 different rat strains also revealed a
             significant correlation between increase in DFI in the
             presence of saccharin and ethanol intake. These findings
             suggest that the dramatic increase in of DFI in the presence
             of saccharin may be an animal analog of the clinical
             phenomenon known as a loss of control.},
   Language = {eng},
   Key = {fds275632}
}

@article{fds275631,
   Author = {Rezvani, AH and Grady, DR and Peek, AE and Pucilowski,
             O},
   Title = {Inhibition of nitric oxide synthesis attenuates alcohol
             consumption in two strains of alcohol-preferring
             rats.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {50},
   Number = {2},
   Pages = {265-270},
   Year = {1995},
   Month = {February},
   ISSN = {0091-3057},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7537886},
   Keywords = {Alcohol Drinking • Amino Acid Oxidoreductases •
             Animals • Arginine • Body Temperature •
             Dose-Response Relationship, Drug • Ethanol • Heart
             Rate • Male • Motor Activity •
             NG-Nitroarginine Methyl Ester • Nitric Oxide •
             Nitric Oxide Synthase • Rats • Species Specificity
             • analogs & derivatives* • antagonists &
             inhibitors • antagonists & inhibitors* •
             biosynthesis* • blood • drug effects •
             genetics • pharmacology • psychology*},
   Abstract = {The effect of the nitric oxide synthase inhibitor
             NG-nitro-L-arginine methyl ester (L-NAME) on voluntary
             alcohol consumption was examined in two different strains of
             alcohol-preferring rats, in a continuous-access,
             two-bottle-choice paradigm. Compared with the vehicle,
             intraperitoneal injections of L-NAME significantly and
             dose-dependently (10, 30, and 60 mg/kg) suppressed alcohol
             intake and preference in both alcohol-preferring (P) and
             Fawn-Hooded (FH) rats. The effect of the highest dose of
             L-NAME was nonspecific; it caused general decreases in
             consumption of alcohol, water, and food. Repeated injection
             of L-NAME (30 mg/kg) for 4 consecutive days significantly
             attenuated alcohol intake, but tolerance developed after 3
             days of treatment. A single administration of a high dose of
             L-NAME (60 mg/kg) did not influence the blood alcohol
             concentrations, which suggests a possible central effect.
             Furthermore, a moderate dose of 30 mg/kg L-NAME, which
             selectively inhibited alcohol intake, did not exert a
             significant effect on telemetrically measured heart rate,
             core body temperature, and gross motor activity of alcohol
             naive Fawn-Hooded rats. These results suggest an involvement
             of nitric oxide in alcohol drinking behavior. Although the
             true mechanism(s) of action is not yet clear, it can be
             speculated that L-NAME may exert its action indirectly by
             modulating neurotransmitters proposed to be involved in
             alcohol drinking and/or by influencing other neuronal
             factors, such as neuronal Ca2+ channels, which have been
             shown to be involved in alcohol drinking
             behavior.},
   Language = {eng},
   Key = {fds275631}
}

@article{fds275629,
   Author = {Ayensu, WK and Pucilowski, O and Mason, GA and Overstreet, DH and Rezvani, AH and Janowsky, DS},
   Title = {Effects of chronic mild stress on serum complement activity,
             saccharin preference, and corticosterone levels in Flinders
             lines of rats.},
   Journal = {Physiology & Behavior},
   Volume = {57},
   Number = {1},
   Pages = {165-169},
   Year = {1995},
   Month = {January},
   ISSN = {0031-9384},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7878112},
   Keywords = {Animals • Complement Activation • Complement
             System Proteins • Corticosterone • Food
             Preferences* • Hemolytic Plaque Technique •
             Immunoassay • Male • Rats • Saccharin •
             Stress, Psychological • analysis* • blood* •
             immunology • metabolism*},
   Abstract = {Complement proteins and fragments participate in the
             induction and modulation of specific and nonspecific immune
             reactions. We have examined the effect of 4 weeks of chronic
             mild stress (CMS) on complement sheep red blood cell
             hemolytic activity measured in CH50 units in two selectively
             bred lines of rats, the Flinders resistant line (FRL) and
             the Flinders sensitive line (FSL), that differ in
             cholinergic sensitivity and behavioral characteristics.
             Additionally, CMS-induced hedonic deficit (decreased
             preference for 0.02% saccharin over water) and serum
             corticosterone levels were compared in FRL and FSL rats. CMS
             caused a significantly (p < 0.01) greater decline in CH50
             responses in FSL (-15%) than in FRL (-7%) rats. This was
             accompanied by a significant (p < 0.01) suppression of
             saccharin preference over a 24 h period in both FRL and FSL
             rats. Both lines showed a similar, more than 2-fold (p <
             0.01) increase in corticosterone levels following CMS. These
             results further confirm that CMS induces a depressive-like
             state in rats as well as the validity of the FSL rat as a
             genetic model of depression. They also indicate that the
             effect of stress on the immune system can be monitored by
             measuring the complement CH50 response.},
   Language = {eng},
   Key = {fds275629}
}

@article{fds275622,
   Author = {Mason, GA and Rezvani, AH and Grady, DR and Garbutt,
             JC},
   Title = {The subchronic effects of the TRH analog TA-0910 and
             bromocriptine on alcohol preference in alcohol-preferring
             rats: development of tolerance and cross-tolerance.},
   Journal = {Alcoholism, Clinical and Experimental Research},
   Volume = {18},
   Number = {5},
   Pages = {1196-1201},
   Year = {1994},
   Month = {October},
   ISSN = {0145-6008},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7847606},
   Keywords = {Alcohol Drinking • Alcoholism • Animals •
             Bromocriptine • Dopamine • Dose-Response
             Relationship, Drug • Drug Tolerance • Injections,
             Subcutaneous • Male • Rats • Rats, Inbred
             Strains • Thyrotropin-Releasing Hormone • analogs
             & derivatives* • pharmacology • pharmacology*
             • physiology • physiology* •
             physiopathology*},
   Abstract = {In a previous study, we showed that a single injection of
             the thyrotropin-releasing hormone analog TA-0910
             dose-dependently reduced alcohol intake in
             alcohol-preferring (P) rats and increased their water intake
             over a 24-hr period. In the present study, the effects of
             seven consecutive, once-daily injections of TA-0910 (0.75
             mg/kg, ip) on alcohol preference were determined. P rats
             developed tolerance to the attenuating effects of TA-0910 on
             alcohol intake within 3-5 days. Following the development of
             tolerance to TA-0910, rats were injected with the dopamine
             agonist bromocriptine (0.5 mg/kg, sc). In the presence of
             tolerance to TA-0910, the attenuating effect of
             bromocriptine on alcohol intake was reduced. When rats were
             made tolerant to the attenuating effects of bromocriptine,
             they exhibited tolerance to the attenuating effects of
             TA-0910. These findings indicate that tolerance to the
             effects of TA-0910 on alcohol intake occurs and suggest
             dopamine involvement in the mechanism of action of TA-0910
             in reducing alcohol intake in P rats.},
   Language = {eng},
   Key = {fds275622}
}

@article{fds275625,
   Author = {Criswell, HE and Overstreet, DH and Rezvani, AH and Johnson, KB and Simson, PE and Knapp, DJ and Moy, SS and Breese, GR},
   Title = {Effects of ethanol, MK-801, and chlordiazepoxide on
             locomotor activity in different rat lines: dissociation of
             locomotor stimulation from ethanol preference.},
   Journal = {Alcoholism, Clinical and Experimental Research},
   Volume = {18},
   Number = {4},
   Pages = {917-923},
   Year = {1994},
   Month = {August},
   ISSN = {0145-6008},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7978104},
   Keywords = {Alcohol Drinking • Animals • Arousal •
             Chlordiazepoxide • Dizocilpine Maleate •
             Dose-Response Relationship, Drug • Ethanol • Male
             • Motor Activity • Rats • Rats, Inbred
             Strains • Receptors, GABA-A • Receptors,
             N-Methyl-D-Aspartate • Species Specificity • drug
             effects • drug effects* • genetics* •
             pharmacology • pharmacology*},
   Abstract = {Several lines of research have suggested a link between the
             reward value of a drug and its ability to stimulate
             locomotion. One goal of the present study was to determine
             whether ethanol preferentially stimulates locomotor activity
             in lines of rat that show a preference for ethanol. A
             secondary goal was to determine the extent to which the
             benzodiazepine-like and NMDA antagonistic action of ethanol
             accounted for its effect on locomotor activity. To meet
             these goals, the effects of varying doses of ethanol
             (0.125-1.0 g/kg), MK-801 (0.1-0.3 mg/kg), and
             chlordiazepoxide (0.3-3 mg/kg) on locomotor activity were
             studied in several lines of rats that had been habituated to
             the testing procedure. The effect of low doses of ethanol on
             motor activity in the Alcohol-Preferring (P) and Fawn-Hooded
             rats, which show a strong ethanol preference, were similar
             to those of the alcohol-nonpreferring (NP), Flinders
             Sensitive Line, and Flinders Resistant Line rats. Only the
             Flinder Resistant Line rats showed a small, but significant
             increase in locomotor activity after the administration of
             ethanol. The highest dose of ethanol (1.0 g/kg) produced
             locomotor depression in all lines except the P and NP lines,
             which were not tested at this dose. These findings do not
             support a link between locomotor stimulation by ethanol and
             ethanol preference. In contrast, all lines exhibited
             locomotor stimulation after moderate (0.1-0.3 mg/kg) doses
             of MK-801, but did not exhibit increases in activity
             following any dose of chlordiazepoxide. These data indicate
             that the profiles of activity after MK-801 and
             chlordiazepoxide were distinct from that of ethanol in the
             various rat lines.(ABSTRACT TRUNCATED AT 250
             WORDS)},
   Language = {eng},
   Doi = {10.1111/j.1530-0277.1994.tb00060.x},
   Key = {fds275625}
}

@article{fds275628,
   Author = {Rezvani, AH and Overstreet, DH and Ejantkar, A and Gordon,
             CJ},
   Title = {Autonomic and behavioral responses of selectively bred
             hypercholinergic rats to oxotremorine and diisopropyl
             fluorophosphate.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {48},
   Number = {3},
   Pages = {703-707},
   Year = {1994},
   Month = {July},
   ISSN = {0091-3057},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7938125},
   Keywords = {Animals • Autonomic Nervous System • Behavior,
             Animal • Body Temperature • Circadian Rhythm
             • Heart Rate • Isoflurophate • Male •
             Motor Activity • Oxotremorine • Parasympathetic
             Nervous System • Rats • Species Specificity •
             drug effects • drug effects* • pharmacology*
             • physiology • physiology*},
   Abstract = {The hypercholinergic Flinders Sensitive Line (FSL) rat was
             significantly more sensitive than the Flinders Resistant
             Line (FRL) rat to the biotelemetrically recorded hypothermic
             effects of oxotremorine, a direct-acting muscarinic agonist,
             and diisopropyl fluorophosphate (DFP), an anticholinesterase
             agent. The effects of these agents on heart rate and motor
             activity, also recorded biotelemetrically, indicate either
             small differences (DFP) or no significant effect
             (oxotremorine) between the lines. These findings confirm the
             dramatic differences in temperature responses to cholinergic
             compounds between FSL and FRL rats, for which they were
             selectively bred, but suggest that a general increase in the
             sensitivity of the FSL rats to all muscarinic-mediated
             responses may not occur.},
   Language = {eng},
   Key = {fds275628}
}

@article{fds275627,
   Author = {Rezvani, AH and Grady, DR},
   Title = {Suppression of alcohol consumption by fenfluramine in
             Fawn-Hooded rats with serotonin dysfunction.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {48},
   Number = {1},
   Pages = {105-110},
   Year = {1994},
   Month = {May},
   ISSN = {0091-3057},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8029280},
   Keywords = {Alcohol Deterrents • Alcohol Drinking • Animals
             • Dose-Response Relationship, Drug • Drinking
             • Eating • Ethanol • Fenfluramine • Male
             • Rats • Rats, Inbred Strains • Rats,
             Sprague-Dawley • Serotonin • blood • drug
             effects • genetics • pharmacology* •
             physiology* • psychology*},
   Abstract = {The high preference for alcohol intake observed in
             Fawn-Hooded rats has been attributed to the central
             serotonin (5-HT) dysfunction in this strain. To further
             characterize the involvement of 5-HT in alcohol-seeking
             behavior in Fawn-Hooded rats, the effect of both acute and
             subchronic administration of fenfluramine, a 5-HT releaser,
             on alcohol intake and preference was determined. Rats were
             individually housed and provided free access to a solution
             of 10% alcohol, food, and water. After establishing a stable
             baseline, rats were injected twice daily for 1 day or for 5
             consecutive days either with saline or 0.1, 0.25, 0.5, and
             1.0 mg/kg of fenfluramine at 0930 h and 1600 h, and their
             consumption of alcohol, food, and water was measured for 24
             h. Another group of rats scheduled with a limited access (1
             h/day) to alcohol and free access to food and water were
             injected with either saline or 0.25, 0.5, 0.75, and 1.0
             mg/kg fenfluramine 20 min before exposure to alcohol, and
             their alcohol consumption was measured at the end of 1 h
             exposure. Further, to determine the effect of fenfluramine
             on alcohol metabolism, rats were injected with 1.0 mg/kg
             fenfluramine or saline and 15 min later with 2.5 g/kg
             alcohol (16%, v/v). Blood alcohol levels were then measured
             at 1, 3, and 5 h after alcohol administration. Our results
             demonstrate that both acute and subchronic administration of
             fenfluramine dose-dependently attenuate alcohol intake and
             increased water intake without a significant effect on food
             intake. Fenfluramine did not affect the pharmacokinetics of
             alcohol, indicating a central effect.(ABSTRACT TRUNCATED AT
             250 WORDS)},
   Language = {eng},
   Key = {fds275627}
}

@article{fds275623,
   Author = {Pucilowski, O and Rezvani, AH and Overstreet, DH and Janowsky,
             DS},
   Title = {Calcium channel inhibitors attenuate consumption of ethanol,
             sucrose and saccharin solutions in rats},
   Journal = {Behavioural Pharmacology},
   Volume = {5},
   Number = {4-5},
   Pages = {494-501},
   Year = {1994},
   Month = {January},
   ISSN = {0955-8810},
   url = {http://dx.doi.org/10.1097/00008877-199408000-00010},
   Abstract = {Ca2+ channel inhibitors suppress ethanol intake in various
             strains of alcohol-preferring rats. To test whether that
             inhibitory effect involves interference with the caloric
             consequences of preferred fluids, we compared the effects of
             two dihydropyridines, nicardipine and isradipine, and
             diltiazem, a benzothiazepine Ca2+ channel inhibitor, on
             intake of and preference for 10% ethanol (v/v), 13.7%
             sucrose (w/v, isocaloric to 10% ethanol) and non-caloric
             0.02% saccharin (w/v) solutions. All of these Ca2+ channel
             inhibitors dose-dependently (1.25-5 μmol/kg isradipine,
             5-20 μmol/kg nicardipine, 10-40 μmol/kg diltiazem)
             inhibited ethanol intake in alcohol-preferring P rats.
             Nicardipine and isradipine, but not diltiazem,
             simultaneously increased water intake and attenuated
             preference for ethanol. No change in food pellet intake was
             found. Similar inhibition was observed with regard to
             sucrose and saccharin intake in Sprague-Dawley rats,
             although higher doses (> 10 μmol/kg) were required to
             achieve that effect. No significant changes in sucrose
             preference, as opposed to consumption, were observed with
             any drug, and only nicardipine at its highest dose (20
             μmol/kg, b.i.d.) significantly (p < 0.05) decreased
             preference for saccharin. In conclusion, all three Ca2+
             channel inhibitors significantly suppress consumption of
             caloric solutions of ethanol and sucrose, as well as of
             non-caloric saccharin solution. Although an accompanying
             decrease in preference is evident only for alcohol, it
             appears that these effects may be related to decreased
             palatability of flavored fluids. However, the contribution
             of changes in ethanol- and sucrose-induced caloric satiety
             cannot be ruled out.},
   Language = {ENG},
   Doi = {10.1097/00008877-199408000-00010},
   Key = {fds275623}
}

@article{fds275624,
   Author = {Overstreet, DH and Janowsky, DS and Pucilowski, O and Rezvani,
             AH},
   Title = {Swim test immobility co-segregates with serotonergic but not
             cholinergic sensitivity in cross-breeds of Flinders Line
             rats.},
   Journal = {Psychiatric Genetics},
   Volume = {4},
   Number = {2},
   Pages = {101-107},
   Year = {1994},
   ISSN = {0955-8829},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8055248},
   Keywords = {8-Hydroxy-2-(di-n-propylamino)tetralin • Analysis of
             Variance • Animals • Depressive Disorder •
             Disease Models, Animal • Female • Hypothermia
             • Male • Oxotremorine • Rats •
             Receptors, Cholinergic • Receptors, Serotonin •
             Swimming • chemically induced • genetics* •
             pharmacology • physiopathology},
   Abstract = {The Flinders Sensitive Line (FSL) rat, a genetic animal
             model of depression, was cross-bred with its normal control,
             the Flinders Resistant Line (FRL) rat, in order to
             investigate the relationship between cholinergic
             sensitivity, the selected variable, and two apparent
             genetically correlated variables, serotonergic sensitivity
             and swim test immobility. Cross-breeding established F1, F2
             and back-cross progeny, with at least 20 rats of each sex
             for each group. Cholinergic sensitivity was assessed as the
             hypothermic response to oxotremorine (0.2 mg/kg) in 30 day
             old rats. Serotonergic sensitivity was assessed as the
             hypothermic response to 8-OH-DPAT, a serotonin (5-HT)-1A
             agonist, in 35-40 day old rats. Immobility was assessed as
             the time spent immobile in a 5 min swim test in 60-70 day
             old rats. For each variable, there were highly significant
             group differences, with the parental FSL and FRL groups
             being at the extremes. The segregating populations tended to
             be intermediate between the parental lines and were
             generally significantly different from both FSL and FRL
             groups. However, the crosses more closely resembled the FRL
             parent for only the cholinergic responses, the distributions
             for 8-OH-DPAT and immobility suggesting predominantly
             additive genetics. Statistical analyses with chi square to
             compare response distributions and regression to quantify
             the association between variables in the segregating
             populations confirmed that cholinergic sensitivity was
             different from serotonergic sensitivity and immobility,
             which were significantly correlated with each
             other.(ABSTRACT TRUNCATED AT 250 WORDS)},
   Language = {eng},
   Key = {fds275624}
}

@article{fds275626,
   Author = {Overstreet, DH and Rezvani, AH and Pucilowski, O and Gause, L and Janowsky, DS},
   Title = {Rapid selection for serotonin-1A sensitivity in
             rats.},
   Journal = {Psychiatric Genetics},
   Volume = {4},
   Number = {1},
   Pages = {57-62},
   Year = {1994},
   ISSN = {0955-8829},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8049904},
   Keywords = {8-Hydroxy-2-(di-n-propylamino)tetralin • Analysis of
             Variance • Animals • Body Temperature •
             Breeding* • Female • Male • Oxotremorine
             • Rats • Receptors, Serotonin • Receptors,
             Serotonin, 5-HT1 • drug effects • genetics* •
             pharmacology},
   Abstract = {National Institutes of Health (NIH) heterogeneous stock (HS)
             rats were obtained and genetically selected for either
             larger (HI line) or smaller (LO line) hypothermic responses
             to the selective serotonin-1A (5-HT1A) agonist
             8-hydroxy-2-(di-N-propylamino)tetralin (8-OH-DPAT). A
             randomly bred (RA) control line was also bred in parallel.
             There was a rapid response to selection, with HI and LO S1
             progeny already showing significantly different hypothermic
             responses to DPAT. The data for the S3 progeny indicated
             that selection was proceeding in both directions, with the
             hypothermic responses of the LO line being about 0.5 degrees
             C less than that of the RA line (p < 0.01) and the
             hypothermic response of the HI line being about 0.7 degrees
             C greater (p < 0.01). The selected lines also differed in
             their hypothermic responses to the cholinergic agonist
             oxotremorine, but these differences did not change with
             further selection. These findings indicate that selection
             for 5-HT1A sensitivity may occur quite rapidly and that
             changes in muscarinic sensitivity do not parallel those
             changes in serotonergic sensitivity.},
   Language = {eng},
   Key = {fds275626}
}

@article{fds275630,
   Author = {Overstreet, DH and Rezvani, AH and Pucilowski, O and Janowsky,
             DS},
   Title = {5-HT receptors: implications for the neuropharmacology of
             alcohol and alcoholism.},
   Journal = {Alcohol and Alcoholism (Oxford, Oxfordshire).
             Supplement},
   Volume = {2},
   Pages = {205-210},
   Year = {1994},
   ISSN = {1358-6173},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8974337},
   Keywords = {Alcohol Drinking • Alcoholism • Animals •
             Brain • Ethanol • Rats • Receptors, Serotonin
             • Serotonin Antagonists • Serotonin Receptor
             Agonists • classification • drug effects •
             drug effects* • metabolism • metabolism* •
             pharmacology • toxicity*},
   Abstract = {The involvement of serotonergic mechanisms in the
             neuropharmacology of alcohol was appreciated before it was
             recognized that there were multiple subtypes of serotonin
             (5-hydroxytryptamine; 5-HT) receptors. Thus, it was known
             that manipulations of the central serotonergic system could
             lead to a modification of the rate of tolerance development
             to alcohol (Frankel et al., 1975) or to a modulation of
             alcohol intake (Myers and Martin, 1973; Myers and Melchior,
             1975) before Peroutka and Snyder (1979) first suggested that
             there were at least two subtypes of 5-HT receptors. Since
             these early reports were written, there has been a wealth of
             studies which have continued to support a role for 5-HT in
             the regulation of alcohol intake (See McBride et al., 1993b;
             Sellers et al., 1992, for reviews). Simultaneously, a
             tremendous expansion in the number of known 5-HT receptor
             subtypes has occurred (See Peroutka, 1988). However, there
             have not been, to our knowledge, any papers which have
             examined the possible role of specific 5-HT receptor
             subtypes in the regulation of alcohol's central effects. The
             present review addresses this deficiency in the literature.
             This review will focus on three major areas: the
             pharmacological regulation of alcohol intake; differences in
             5-HT receptor subtypes among alcohol-preferring and
             -nonpreferring rat strains; and alterations in 5-HT receptor
             subtypes following chronic exposure to alcohol.},
   Language = {eng},
   Key = {fds275630}
}

@article{fds275621,
   Author = {Pucilowski, O and Overstreet, DH and Rezvani, AH and Janowsky,
             DS},
   Title = {Chronic mild stress-induced anhedonia: greater effect in a
             genetic rat model of depression.},
   Journal = {Physiology & Behavior},
   Volume = {54},
   Number = {6},
   Pages = {1215-1220},
   Year = {1993},
   Month = {December},
   ISSN = {0031-9384},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8295967},
   Keywords = {Animals • Arousal • Depressive Disorder •
             Disease Models, Animal* • Food Preferences • Male
             • Models, Genetic* • Motivation* • Rats
             • Rats, Inbred Strains • Saccharin • Species
             Specificity • Stress, Psychological • Taste •
             complications* • genetics • genetics* •
             psychology},
   Abstract = {The effects of acute and chronic stressors on saccharin
             intake and preference in the hypercholinergic Flinders
             Sensitive Line (FSL) rat, a putative genetic animal model of
             depression, were studied and compared to the control
             Flinders Resistant Line (FRL) rats. Overall, the FRL rats
             drank significantly less saccharin and water than the FSL
             rats when compared over a wide range of saccharin
             concentrations (0.01-5%) under baseline conditions. A 0.02%
             saccharin concentration was used in subsequent experiments.
             We observed a significant suppression of saccharin
             intake/preference at 1 h following a single 5-min exposure
             to cold swim stress only in FSL rats. There was a tendency
             to increase saccharin intake in both lines at 1 h following
             a scrambled foot shock stress. These effects of acute
             stressors disappeared upon retesting for saccharin
             consumption/preference 23 h after the stress. Chronic 4-week
             exposure to unpredictable mild stressors significantly (p <
             0.01) decreased saccharin consumption in the FSL rats, but
             not in the FRL rats. The FSL rats also exhibited a
             significantly greater decrease in saccharin preference (-24%
             vs. prestress baseline, as compared to -7% in FRL controls,
             p < 0.05). In conclusion, FSL rats appear more prone than
             the FRL rats to chronic, as well as immediate acute,
             stress-induced anhedonic effects. This outcome further
             supports the notion that the FSL rat is a useful model of a
             genetic predisposition to depressive-like
             reactions.},
   Language = {eng},
   Key = {fds275621}
}

@article{fds275620,
   Author = {Rezvani, AH and Pucilowski, O and Grady, DR and Janowsky, D and O'Brien,
             RA},
   Title = {Reduction of spontaneous alcohol drinking and physical
             withdrawal by levemopamil, a novel Ca2+ channel antagonist,
             in rats.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {46},
   Number = {2},
   Pages = {365-371},
   Year = {1993},
   Month = {October},
   ISSN = {0091-3057},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8265691},
   Keywords = {Alcohol Drinking • Animals • Biogenic Monoamines
             • Brain Chemistry • Calcium Channel Blockers
             • Dose-Response Relationship, Drug • Eating •
             Ethanol • Male • Rats • Rats, Wistar •
             Substance Withdrawal Syndrome • Verapamil •
             analogs & derivatives* • blood • drug effects
             • metabolism • pharmacokinetics • prevention
             & control* • psychology* • therapeutic use •
             therapeutic use*},
   Abstract = {Neuronal Ca2+ channels have been shown to be involved in
             both alcohol drinking behavior in rats and nonhuman primates
             and in the manifestation of alcohol withdrawal symptoms in
             rodents. Experiments were performed to determine the effect
             of a single injection of levemopamil, a novel Ca2+ channel
             antagonist with antiserotonergic [5-hydroxytryptamine2
             (5-HT2)] properties, on alcohol preference and alcohol
             withdrawal symptoms in alcohol-preferring (P) and Wistar
             rats, respectively. P rats were individually housed and
             provided free access to food, water, and a solution of 10%
             (v/v) ethanol. Ethanol, food, and water intakes were
             measured daily. After establishing a stable baseline, P rats
             were injected with levemopamil (0, 3.3, 10, 15, and 20
             mg/kg) and their food, water, and alcohol intakes measured
             24 h later. In a separate experiment, the ability of acute
             and chronic (12 consecutive days) administrations of
             levemopamil to suppress alcohol withdrawal symptoms in
             chronically alcohol-treated rats was studied. In addition,
             the effects of levemopamil on the level of monoamines in
             different areas of the brain, as well as its action in
             alcohol metabolism, were examined. Our findings showed that
             a single administration of levemopamil (10, 15, and 20
             mg/kg) significantly and dose-dependently attenuated alcohol
             intake and increased water intake in P rats. Both acute and
             chronic treatment with levemopamil reduced the alcohol
             withdrawal symptoms, overall seizure scores, and proportion
             of rats seizing. A single injection of levemopamil produced
             a clear, but not significant, trend to increase the 5-HT
             turnover rate in certain brain areas. This drug did not
             influence the pharmacokinetics of alcohol.(ABSTRACT
             TRUNCATED AT 250 WORDS)},
   Language = {eng},
   Key = {fds275620}
}

@article{fds275618,
   Author = {Pucilowski, O and Garges, PL and Rezvani, AH and Hutheson, S and Janowsky, DS},
   Title = {Verapamil suppresses d-amphetamine-induced place preference
             conditioning.},
   Journal = {European Journal of Pharmacology},
   Volume = {240},
   Number = {1},
   Pages = {89-92},
   Year = {1993},
   Month = {August},
   ISSN = {0014-2999},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8405127},
   Keywords = {Animals • Conditioning (Psychology) •
             Dextroamphetamine • Male • Rats • Rats,
             Wistar • Reinforcement (Psychology)* • Verapamil
             • drug effects* • pharmacology*},
   Abstract = {The effect of pretreatment with (+/-)-verapamil (5, 10 or 15
             mg/kg, i.p.) on place preference induced with d-amphetamine
             (1 mg/kg, i.p. 40 min after verapamil) was studied in male
             rats. Place preference conditioning was performed using
             two-compartment shuttle boxes and 8 alternating
             stimulant/saline sessions. Verapamil dose-dependently
             suppressed amphetamine-induced place preference. No
             significant changes in place preference were observed
             following 8 alternating verapamil (no stimulant)/saline
             sessions, irrespective of whether verapamil injections were
             paired with the originally less or the originally more
             preferred compartment. It appears that verapamil effectively
             suppresses the reinforcing properties of d-amphetamine in
             the paradigm used.},
   Language = {eng},
   Key = {fds275618}
}

@article{fds275619,
   Author = {Overstreet, DH and Kampov-Polevoy, AB and Rezvani, AH and Murrelle,
             L and Halikas, JA and Janowsky, DS},
   Title = {Saccharin intake predicts ethanol intake in genetically
             heterogeneous rats as well as different rat
             strains.},
   Journal = {Alcoholism, Clinical and Experimental Research},
   Volume = {17},
   Number = {2},
   Pages = {366-369},
   Year = {1993},
   Month = {April},
   ISSN = {0145-6008},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/8488981},
   Keywords = {Alcohol Drinking • Animals • Arousal •
             Drinking • Genotype* • Male • Rats •
             Rats, Inbred Strains • Saccharin • Species
             Specificity • Taste • administration & dosage*
             • genetics*},
   Abstract = {Saccharin and ethanol intakes were measured in seven strains
             of rats known to differ in their preferences for ethanol:
             The Fawn-Hooded (FH), alcohol-preferring (P) and Maudsley
             Reactive rats have been reported to drink ethanol
             voluntarily, whereas the alcohol-nonpreferring, Maudsley
             Nonreactive and Flinders Line (FSL and FRL) rats do not.
             Saccharin and ethanol intakes were highly correlated (r =
             +0.61) over all strains, with the FH rats drinking the most
             of both solutions. Correlation coefficients between pairs of
             drinking versus nondrinking rat strains were even higher. In
             a second experiment, genetically heterogeneous F2 progeny
             from cross-breeding the ethanol-preferring FH rats with the
             ethanol-nonpreferring Flinders Resistant Line (FRL) rats
             were studied. The results indicated a high positive
             correlation between saccharin and ethanol intakes (+0.65).
             These findings suggest that the association between
             saccharin and ethanol intakes previously reported in rat
             strains with different preferences for ethanol may have a
             similar genetic basis.},
   Language = {eng},
   Key = {fds275619}
}

@article{fds275617,
   Author = {Rezvani, AH and Garges, PL and Miller, DB and Gordon,
             CJ},
   Title = {Attenuation of alcohol consumption by MDMA (ecstasy) in two
             strains of alcohol-preferring rats.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {43},
   Number = {1},
   Pages = {103-110},
   Year = {1992},
   Month = {September},
   ISSN = {0091-3057},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/1357675},
   Keywords = {3,4-Methylenedioxyamphetamine • Alcohol Drinking •
             Animals • Body Temperature • Drinking Behavior
             • Eating • Male • N-Methyl-3,4-methylenedioxyamphetamine
             • Rats • Rats, Inbred Strains • Serotonin
             • Species Specificity • analogs & derivatives*
             • drug effects • genetics* • pharmacology
             • physiology • psychology},
   Abstract = {Alcohol preference and manifestation of alcoholism are
             thought by many to be associated with serotonin (5-HT)
             dysfunction in the brain. Thus, experiments were performed
             to determine the effect of acute and subchronic
             administration of (+/-) 3,4-methylenedioxymethamphetamine
             (MDMA), an amphetamine analog that stimulates 5-HT release,
             on alcohol preference in two strains of alcohol-preferring
             rats, the Fawn-Hooded (FH) and alcohol-preferring (P) rats.
             Rats were individually housed and provided free access to a
             solution of 10% ethanol, food, and water. Ethanol, food, and
             water intakes were measured daily. After establishing a
             stable baseline for ethanol and water intake, each rat was
             injected SC with a dose of 5.0 mg/kg MDMA or an equal volume
             of saline for 1 or 3 consecutive days. Body temperature was
             recorded immediately before and 120, 240, and 360 min after
             MDMA treatment. Ethanol, food, and water intake were
             measured for the preceding 24 h. Further, to determine the
             effect of MDMA on alcohol metabolism rats were injected with
             5.0 mg/kg MDMA or saline and 15 min later with 2.5 g/kg
             alcohol. Then, blood alcohol levels were determined at 1, 3,
             and 5 h after alcohol administration. Our results show that
             a single administration of 5.0 mg/kg MDMA significantly
             decreased ethanol intake in both FH and P rats and increased
             water intake. Subchronic administration of 5.0 mg/kg MDMA
             for 3 consecutive days significantly attenuated alcohol
             intake in both strains but only increased water intake in P
             rats. Administration of MDMA induced hyper- and hypothermia
             in FH and P rats, respectively. This drug failed to exert
             any significant effect on the pharmacokinetics of alcohol,
             indicating a central effect.(ABSTRACT TRUNCATED AT 250
             WORDS)},
   Language = {eng},
   Key = {fds275617}
}

@article{fds275616,
   Author = {Overstreet, DH and Rezvani, AH and Janowsky, DS},
   Title = {Maudsley reactive and nonreactive rats differ only in some
             tasks reflecting emotionality.},
   Journal = {Physiology & Behavior},
   Volume = {52},
   Number = {1},
   Pages = {149-152},
   Year = {1992},
   Month = {July},
   ISSN = {0031-9384},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/1528998},
   Keywords = {Animals • Anxiety • Avoidance Learning •
             Behavior, Animal • Emotions • Male • Rats
             • Rats, Inbred Strains • Species Specificity
             • Swimming • physiology • physiology* •
             psychology},
   Abstract = {The behavior of Maudsley reactive and nonreactive rats,
             along with that of Wistar controls, was studied using three
             behavioral tasks which have been associated with
             emotionality. Consistent with the hypothesis that they are
             more emotional, the Maudsley reactive rats were more
             immobile in the forced swim test and spent less time in the
             open arms of an elevated plus maze than the Maudsley
             nonreactive or Wistar control rats. However, they learned a
             two-way active avoidance task just as well as the other two
             groups. These findings suggest that emotionality is
             heterogeneous and/or that it is involved to different
             degrees in the three behavioral tasks.},
   Language = {eng},
   Key = {fds275616}
}

@article{fds275614,
   Author = {Overstreet, DH and Rezvani, AH and Janowsky, DS},
   Title = {Genetic animal models of depression and ethanol preference
             provide support for cholinergic and serotonergic involvement
             in depression and alcoholism.},
   Journal = {Biological Psychiatry},
   Volume = {31},
   Number = {9},
   Pages = {919-936},
   Year = {1992},
   Month = {May},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/1386257},
   Keywords = {8-Hydroxy-2-(di-n-propylamino)tetralin • Alcohol
             Drinking • Alcoholism • Animals • Arousal
             • Avoidance Learning • Brain • Buspirone
             • Crosses, Genetic • Depressive Disorder •
             Discrimination Learning • Escape Reaction • Mental
             Recall • Models, Genetic* • Orientation •
             Oxotremorine • Piperazines • Rats • Rats,
             Inbred Strains • Receptors, Cholinergic •
             Receptors, Serotonin • Tetrahydronaphthalenes •
             drug effects • genetics* • pharmacology •
             physiology • physiopathology},
   Abstract = {The present article summarizes some comparative studies of
             the Fawn-Hooded (FH) rat, a potential animal model of
             ethanol preference, and the Flinders Sensitive Line (FSL)
             rat, a potential animal model of depression. Both FH and FSL
             rats exhibit high degrees of immobility in the forced swim
             test and have difficulty learning a two-way active avoidance
             task. However, there were no differences between the FH and
             FSL rats in the elevated plus maze. Studies of ethanol
             preference indicated high rates of ethanol intake (greater
             than 4 g/kg) and preference (greater than 50%) in the FH
             rats, but low rates of ethanol intake (less than 1.1 g/kg)
             and preference (less than 20%) in FSL rats. It is concluded
             that the FSL rats exhibit behaviors consistent with their
             being an animal model of depression, whereas the FH rats
             exhibit features consistent with their being an animal model
             of both depression and alcoholism. Psychopharmacological
             challenges indicated that both FSL and FH rats were more
             sensitive to the hypothermic effects of oxotremorine, a
             muscarinic agonist. However, FSL rats were also more
             sensitive to serotonergic agonists, and some of the present
             results and other investigators have reported serotonergic
             subsensitivity in the FH rats. Thus, FSL rats exhibit both
             cholinergic and serotonergic supersensitivity, whereas FH
             rats exhibit cholinergic supersensitivity but normal or
             reduced serotonergic sensitivity. Progeny from a genetic
             cross between FH and FSL rats exhibit cholinergic
             supersensitivity and have high ethanol preference scores.
             These data are consistent with genetic models suggesting
             that ethanol preference may be influenced by dominant genes,
             whereas cholinergic sensitivity may be influenced by
             recessive genes.},
   Language = {eng},
   Key = {fds275614}
}

@article{fds275615,
   Author = {Rezvani, AH and Garbutt, JC and Shimoda, K and Garges, PL and Janowsky,
             DS and Mason, GA},
   Title = {Attenuation of alcohol preference in alcohol-preferring rats
             by a novel TRH analogue, TA-0910.},
   Journal = {Alcoholism, Clinical and Experimental Research},
   Volume = {16},
   Number = {2},
   Pages = {326-330},
   Year = {1992},
   Month = {April},
   ISSN = {0145-6008},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/1590553},
   Keywords = {Alcohol Drinking • Animals • Dose-Response
             Relationship, Drug • Drinking • Male • Rats
             • Rats, Inbred Strains • Thyrotropin-Releasing
             Hormone • analogs & derivatives* • drug effects
             • pharmacology • physiology •
             physiopathology*},
   Abstract = {Experiments were performed to characterize the acute effect
             of different doses of a novel thyrotropin-releasing hormone
             (TRH) analogue (TA-0910) on ethanol intake in rats.
             Selectively bred alcohol-preferring (P) rats received a
             single intraperitoneal injection of normal saline or 0.083,
             0.25 and 0.75 mg/kg of TA-0910 at 9:30 AM, and their
             consumption of ethanol, water, and food was measured for 24
             hr. TA-0910 dose-dependently attenuated ethanol intake and
             commensurately increased water consumption. Only the highest
             dose of TA-0910 increased the total caloric intake. TA-0910
             did not affect the pharmacokinetics of ethanol. These
             findings indicate involvement of TRH systems in ethanol
             preference and suggest that centrally acting TRH analogues
             may be therapeutic in the treatment of alcoholism.},
   Language = {eng},
   Key = {fds275615}
}

@article{fds216591,
   Author = {O Pucilowski and B Eichelman and DH Overstreet and AH Rezvani and DS
             Janowsky},
   Title = {Enhanced affective aggression in genetically bred
             hypercholinergic rats.},
   Journal = {Neuropsychobiology},
   Volume = {24},
   Number = {1},
   Pages = {37-41},
   Year = {1992},
   Month = {January},
   ISSN = {0302-282X},
   Keywords = {Acetylcholine • Aggression • Animals •
             Apomorphine • Depression • Electroshock •
             Male • Pain • Rats • Reaction Time •
             Sensory Thresholds • drug effects • pharmacology
             • physiology • physiology* • physiopathology
             • psychology},
   Abstract = {Affective aggression was studied in pairs of Flinders
             Sensitive Line hypercholinergic rats (FSL) and Flinders
             Resistant Line (FRL) rats in shock-induced and
             apomorphine-induced fighting tests. FSL rats were
             significantly more aggressive in both tests. They had higher
             pain threshold, assessed by the jump-flinch method, than FRL
             rats. It is concluded that genetically developed cholinergic
             system supersensitivity has resulted in enhanced
             responsiveness to stimuli eliciting affective
             aggression.},
   Language = {eng},
   Key = {fds216591}
}

@article{fds275613,
   Author = {Ayensu, WK and Rezvani, AH and Overstreet, DH and Pucilowski, O and Janowsky, DS},
   Title = {Ethanol and complement hemolytic activity of selectively
             bred hypercholinergic rats.},
   Journal = {Alcohol and Alcoholism (Oxford, Oxfordshire)},
   Volume = {27},
   Number = {1},
   Pages = {47-54},
   Year = {1992},
   Month = {January},
   ISSN = {0735-0414},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/1580928},
   Keywords = {Alcoholism • Animals • Complement Hemolytic
             Activity Assay* • Depression • Ethanol •
             Immune Tolerance • Rats • Rats, Inbred Strains
             • Receptors, Cholinergic • immunology •
             immunology* • pharmacokinetics •
             physiology*},
   Abstract = {Depression and alcoholism are associated with impaired
             immune responses. Complement proteins and fragments
             participate in the induction and modulation of both specific
             and non-specific immune reactions. This study examined the
             effect of prolonged ethanol ingestion on complement CH50
             levels in two strains of rats, the Flinders Resistant Line
             (FRL) and the Flinders Sensitive Line (FSL), that differ in
             cholinergic sensitivity and depressive tendencies. Chronic
             ethanol exposure given as either the source of drinking
             fluid or as a liquid diet had a significant inhibition on
             mean CH50 unit responses in both FSL (41-48%) and FRL
             (23-24%) rats. The difference in group response to ethanol
             was confirmed by a significant interaction of ethanol
             treatment versus group in the two-way ANOVA. The FSL rats
             appear to be more easily affected than FRLs. Genetic
             differences in the neurotransmitter systems, therefore, may
             play a role in susceptibility to immunosuppression resulting
             from ethanol exposure.},
   Language = {eng},
   Key = {fds275613}
}

@article{fds275611,
   Author = {Pucilowski, O and Rezvani, AH and Janowsky, DS},
   Title = {Suppression of alcohol and saccharin preference in rats by a
             novel Ca2+ channel inhibitor, Goe 5438.},
   Journal = {Psychopharmacology},
   Volume = {107},
   Number = {2-3},
   Pages = {447-452},
   Year = {1992},
   ISSN = {0033-3158},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/1615142},
   Keywords = {Alcohol Drinking • Animals • Appetite Depressants
             • Calcium Channel Blockers • Dose-Response
             Relationship, Drug • Eating • Ethanol • Male
             • Naphthyridines • Rats • Rats, Inbred
             Strains • Saccharin • drug effects •
             pharmacology • pharmacology* •
             psychology*},
   Abstract = {The effect of the novel 1,4-dihydronaphthyridine Ca2+
             channel inhibitor Goe 5438 (CI-951) on voluntary ethanol
             consumption was examined in selectively bred
             alcohol-preferring (P) rats in a free choice two bottle
             preference test versus water. Intraperitoneally injected Goe
             5438 dose-dependently (5, 10 or 20 mumol/kg, twice daily)
             inhibited ethanol and increased water intake over the 24 h
             period (injection day). The drug decreased ethanol
             preference, originally above 90%, by 6%, 19% and 45% at
             respective doses, on the injection day. That inhibitory
             effect of the highest dose of Goe 5438 on ethanol preference
             remained significant also on days 2 and 3 after injections
             (-51% and -18%, respectively). Goe 5438, in the highest
             dose, also tended to decrease granulated chow consumption
             during the injection day only. To further test whether the
             inhibition of ethanol preference is secondary to decrease in
             reinforcing properties of ethanol and not due to
             interference with satiety mechanisms, we compared the effect
             of two higher doses (10 and 20 mumol/kg, intraperitoneally,
             twice daily) of Goe 5438 on spontaneous preference for a
             non-caloric 0.04% saccharin solution in Sprague-Dawley rats.
             We observed a dose-dependent suppression of preference (by
             44% and 58%, respectively) during the injection day, but not
             the subsequent 24 h period. However, Goe 5438 also
             significantly alleviated food pellet intake on the injection
             day. In conclusion, Goe 5438 produces potent and
             long-lasting inhibition of voluntary ethanol consumption,
             which may be secondary to attenuation of reinforcing
             properties of ethanol.(ABSTRACT TRUNCATED AT 250
             WORDS)},
   Language = {eng},
   Key = {fds275611}
}

@article{fds275607,
   Author = {Pucilowski, O and Overstreet, DH and Rezvani, AH and Janowsky,
             DS},
   Title = {Effects of calcium channel inhibitors on the hypothermic
             response to oxotremorine in normo and hypercholinergic
             rats.},
   Journal = {The Journal of Pharmacy and Pharmacology},
   Volume = {43},
   Number = {6},
   Pages = {436-439},
   Year = {1991},
   Month = {June},
   ISSN = {0022-3573},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/1681059},
   Keywords = {Animals • Apomorphine • Atropine Derivatives
             • Body Temperature • Calcium Channel Blockers
             • Dopamine Agents • Ergolines • Male •
             Oxotremorine • Parasympathetic Nervous System •
             Piperazines • Quinpirole • Rats • Rats,
             Inbred Strains • Receptors, N-Methyl-D-Aspartate •
             antagonists & inhibitors • drug effects* •
             pharmacology • pharmacology* •
             physiology*},
   Abstract = {The Flinders Sensitive Line of rats (FSL) has been
             selectively bred to have increased sensitivity to
             cholinergic drugs. Typically, these rats react with twice as
             great a hypothermic effect to muscarinic agonists such as
             oxotremorine, as do similarly bred Flinders Resistant Line
             rats (FRL). We compared the effects of three chemically
             different calcium channel inhibitors (diltiazem, nicardipine
             and verapamil) on the hypothermia induced in FRL and FSL
             rats by oxotremorine (0.2 mg kg-1 s.c.). Each drug was
             injected i.p. in a dose of 20 mumol kg-1 30 min before
             oxotremorine. Methylatropine (2 mg kg-1 s.c.) was
             administered 15 min before oxotremorine to block the
             peripheral effects of the agonist. The hypothermic effect of
             oxotremorine in FSL rats was antagonized by nicardipine and
             diltiazem. In contrast, verapamil failed to influence the
             hypothermic response in FSL rats. Verapamil significantly (P
             less than 0.05) augmented oxotremorine hypothermia in FRL
             rats. Diltiazem and nicardipine were without effect on
             oxotremorine-induced hypothermia in FRL rats. There were no
             significant changes in temperature in separate groups of FRL
             and FSL rats treated with calcium channel inhibitors
             alone.},
   Language = {eng},
   Key = {fds275607}
}

@article{fds275609,
   Author = {Pucilowski, O and Danysz, W and Overstreet, DH and Rezvani, AH and Eichelman, B and Janowsky, DS},
   Title = {Decreased hyperthermic effect of MK-801 in selectively bred
             hypercholinergic rats.},
   Journal = {Brain Research Bulletin},
   Volume = {26},
   Number = {4},
   Pages = {621-625},
   Year = {1991},
   Month = {April},
   ISSN = {0361-9230},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/1868361},
   Keywords = {Animals • Binding Sites • Body Temperature •
             Body Temperature Regulation* • Cerebral Cortex •
             Dizocilpine Maleate • Hippocampus • Male •
             Rats • Rats, Inbred Strains • Scopolamine
             Hydrobromide • drug effects* • metabolism •
             pharmacology • pharmacology*},
   Abstract = {The Flinders Sensitive Line (FSL) of rats has been
             selectively bred to have increased sensitivity to
             cholinergic agonists. However, these rats exhibit altered
             responsiveness to a number of noncholinergic agents, such as
             apomorphine, buspirone and ethanol. This study compared the
             FSL and control Flinders Resistant Line (FRL) rats in terms
             of their hyperthermic response to the phencyclidine (PCP)
             receptor agonist, MK-801 (0.2 mg/kg SC) and their MK-801
             binding characteristics. We have found that FSL rats react
             with a delayed hyperthermia, having a significantly lower
             hyperthermia for the first 120 min of observation.
             Thereafter the response does not differ in FSL and FRL rats.
             Both groups had similar affinities and numbers of [3H]MK-801
             binding sites in the hippocampus/cerebral cortex.
             Pretreatment with scopolamine (1 mg/kg SC) failed to affect
             MK-801-induced hyperthermia in either line of rats. These
             findings suggest that selective breeding of FSL rats
             attenuated the secondary mechanisms involved in the PCP
             receptor-mediated hyperthermic response. However, by itself
             cholinergic supersensitivity does not appear to be a major
             factor in the blunted responsiveness of FSL rats to
             MK-801.},
   Language = {eng},
   Doi = {10.1016/0361-9230(91)90105-s},
   Key = {fds275609}
}

@article{fds275608,
   Author = {Owens, MJ and Overstreet, DH and Knight, DL and Rezvani, AH and Ritchie,
             JC and Bissette, G and Janowsky, DS and Nemeroff,
             CB},
   Title = {Alterations in the hypothalamic-pituitary-adrenal axis in a
             proposed animal model of depression with genetic muscarinic
             supersensitivity.},
   Journal = {Neuropsychopharmacology},
   Volume = {4},
   Number = {2},
   Pages = {87-93},
   Year = {1991},
   Month = {February},
   ISSN = {0893-133X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/1851013},
   Keywords = {Adrenocorticotropic Hormone • Animals • Brain
             Chemistry • Corticosterone • Corticotropin-Releasing
             Hormone • Depression • Disease Models, Animal
             • Hypothalamo-Hypophyseal System • Male •
             Pituitary Gland, Anterior • Pituitary-Adrenal System
             • Radioimmunoassay • Radioligand Assay • Rats
             • Receptors, Muscarinic • analysis • blood
             • chemistry • genetics • metabolism*},
   Abstract = {Rats from the Flinders Sensitive Line (FSL) and Flinders
             Resistant Line (FRL), which have been bred for differences
             in sensitivity to cholinergic agonists, were killed by
             decapitation under quiet, nonstressful conditions and the
             concentrations of corticotropin-releasing factor (CRF) in
             various brain regions, the concentrations of CRF receptors
             in the anterior pituitary, and plasma ACTH and
             corticosterone concentrations were determined. A first study
             revealed that the cholinergically hypersensitive FSL rats
             exhibited lower concentrations of CRF in the median
             eminence, locus ceruleus, and prefrontal cortex, but no such
             changes in some 13 other brain regions. In this first study,
             the FSL rats had significantly lower plasma ACTH
             concentrations. However, there were no differences in plasma
             corticosterone concentrations between the two groups. A
             second study confirmed the results of the first study and
             revealed that the density of anterior pituitary CRF receptor
             binding sites was elevated in the FSL rats. The observed
             pattern of alterations in these measures of HPA axis
             activity suggest that the cholinergically supersensitive FSL
             rats may possess diminished HPA activity.},
   Language = {eng},
   Key = {fds275608}
}

@article{fds275612,
   Author = {Rezvani, AH and Overstreet, DH and Janowsky, DS},
   Title = {Drug-induced reductions in ethanol intake in alcohol
             preferring and Fawn-Hooded rats.},
   Journal = {Alcohol and Alcoholism (Oxford, Oxfordshire).
             Supplement},
   Volume = {1},
   Pages = {433-437},
   Year = {1991},
   Month = {January},
   ISSN = {1358-6173},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/1845573},
   Keywords = {Alcohol Drinking • Alcoholism • Animals •
             Buspirone • Drinking Behavior • Ethanol •
             Feeding Behavior • Fluoxetine • Male •
             Pindolol • Piperazines • Rats • Rats, Inbred
             Strains • Rats, Wistar • Scopolamine Hydrobromide
             • Self Administration • Serotonin Receptor
             Agonists • Species Specificity • Verapamil •
             administration & dosage • drug effects • genetics
             • pharmacology • pharmacology* • prevention &
             control*},
   Abstract = {The ethanol intake of Fawn-Hooded rats, a serotonin
             deficient strain, was examined under a two bottle choice
             between ethanol (10%) and tap water. The Fawn-Hooded rats
             drank as much ethanol as the alcohol preferring strain of
             rats (approximately 6 times that of the control Wistar
             rats), but drank more fluid and ate more. In general, direct
             and indirect serotonin agonists, reduced ethanol intake to a
             smaller degree in the Fawn-Hooded rats compared to the P
             rats. In contrast the centrally acting antimuscarinic
             scopolamine reduced ethanol intake to a similar degree in
             the two strains.},
   Language = {eng},
   Key = {fds275612}
}

@article{fds275610,
   Author = {Rezvani, AH and Grady, DR and Janowsky, DS},
   Title = {Effect of calcium-channel blockers on alcohol consumption in
             alcohol-drinking monkeys.},
   Journal = {Alcohol and Alcoholism (Oxford, Oxfordshire)},
   Volume = {26},
   Number = {2},
   Pages = {161-167},
   Year = {1991},
   ISSN = {0735-0414},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/1652252},
   Keywords = {Alcohol Drinking • Alcoholism • Animals •
             Brain • Calcium Channels • Diltiazem •
             Dose-Response Relationship, Drug • Female • Macaca
             • Male • Verapamil • drug effects* •
             pharmacology* • physiology • physiopathology
             • physiopathology*},
   Abstract = {Experiments were performed to determine the effect of the
             calcium-channel blockers verapamil and diltiazem on ethanol
             preference in monkeys. Two days of administration of 10
             mg/kg verapamil but not diltiazem or saline significantly
             decreased ethanol intake in all monkeys tested. Chronic
             treatment with verapamil, but not saline, dose-dependently
             attenuated alcohol intake, without significantly influencing
             water intake. These findings suggest that verapamil exerts
             an inhibitory action on ethanol preference in chronically
             alcohol-drinking monkeys, possibly by interfering with
             Ca(2+)-channels and/or by interacting with the activity of
             certain central neurotransmitters.},
   Language = {eng},
   Key = {fds275610}
}

@article{fds275748,
   Author = {Pucilowski, O and Overstreet, DH and Rezvani, AH and Janowsky,
             DS},
   Title = {Effect of verapamil on submissive behavior in genetically
             bred hypercholinergic rats in a water competition
             test.},
   Journal = {European Journal of Pharmacology},
   Volume = {187},
   Number = {3},
   Pages = {507-511},
   Year = {1990},
   Month = {October},
   ISSN = {0014-2999},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2073924},
   Keywords = {Animals • Behavior, Animal • Competitive Behavior
             • Male • Parasympathetic Nervous System •
             Rats • Rats, Inbred Strains • Social Dominance
             • Verapamil • drug effects* •
             pharmacology*},
   Abstract = {Male hypercholinergic FSL (Flinders Sensitive Line) and
             control FRL (Flinders Resistant Line) rats were placed on a
             water deprivation schedule and tested for dominance behavior
             with FSL/FRL pairs competing for water. FSL rats spent
             significantly less time drinking than their FRL partners.
             Acute injection of 10 mg/kg of verapamil, a calcium channel
             inhibitor, to FSL rats markedly increased their drinking
             time without influencing water intake in individually tested
             rats. This effect of the drug was no longer seen after
             prolonged 4 day treatment. It is suggested that
             submissiveness of FSL animals in the water competition test
             might be due to increased fear which is alleviated by
             verapamil treatment. Tolerance seems to develop to this
             effect of the drug.},
   Language = {eng},
   Key = {fds275748}
}

@article{fds275604,
   Author = {Overstreet, DH and Dilsaver, SC and Janowsky, DS and Rezvani,
             AH},
   Title = {Effects of bright light on responsiveness to a muscarinic
             agonist in rats selectively bred for endogenously increased
             cholinergic function.},
   Journal = {Psychiatry Research},
   Volume = {33},
   Number = {2},
   Pages = {139-150},
   Year = {1990},
   Month = {August},
   ISSN = {0165-1781},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2243891},
   Keywords = {Animals • Arousal • Atropine Derivatives •
             Body Temperature Regulation • Hypothalamus •
             Light* • Motor Activity • Oxotremorine •
             Parasympatholytics • Rats • Rats, Inbred Strains
             • Receptors, Muscarinic • Social Environment
             • drug effects • drug effects* • pharmacology
             • pharmacology*},
   Abstract = {The Flinders Sensitive Line (FSL) was derived from the
             Sprague-Dawley rat by selectively breeding those animals
             exhibiting a high level of sensitivity to an
             anticholinesterase. The Flinders Resistant Line (FRL) was
             simultaneously developed as a control line. These lines
             exhibit nonoverlapping distributions of their thermic
             responsiveness to oxotremorine. Bright light prevents the
             development of supersensitivity to oxotremorine occurring as
             a result of forced stress or treatment with a muscarinic
             receptor antagonist in the rat. The authors now report that
             treatment with bright light during the regular photoperiod
             (i.e., a time that does not produce a phase-shift or
             free-running) differentially affects the hypothermic
             response and activity-suppressing effect of oxotremorine in
             both the FSL and FRL. Both lines exhibit decreased
             hypothermia without reduction in motor activity in response
             to oxotremorine following 6 days of treatment with bright
             light. The magnitude of blunting of the hypothermic response
             was greater in the FSL than the FRL. These findings suggest
             that (1) studies of the effects of bright light are
             contingent on the end point one measures and (2) the
             capacity of this treatment to blunt the hypothermic response
             to a muscarinic agonist is greater in an animal model with
             endogenously hyperactive muscarinic cholinergic
             systems.},
   Language = {eng},
   Key = {fds275604}
}

@article{fds275747,
   Author = {Overstreet, DH and Rezvani, AH and Janowsky, DS},
   Title = {Impaired active avoidance responding in rats selectively
             bred for increased cholinergic function.},
   Journal = {Physiology & Behavior},
   Volume = {47},
   Number = {4},
   Pages = {787-788},
   Year = {1990},
   Month = {April},
   ISSN = {0031-9384},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2385654},
   Keywords = {Animals • Arousal • Avoidance Learning •
             Brain • Cholinergic Fibers • Male • Motor
             Activity • Rats • Rats, Inbred Strains •
             Receptors, Cholinergic • Selection, Genetic* •
             Species Specificity* • genetics* • physiology
             • physiology*},
   Abstract = {It was found that the Flinders Sensitive Line (FSL) of rat,
             selectively bred for increased cholinergic function,
             performed poorly in a tone-cued two-way active avoidance
             task in comparison with the control Flinders Restraint Line
             (FRL) of rat. These findings are consistent with the
             suggestion that the FSL rats may be a genetic animal model
             of depression.},
   Language = {eng},
   Key = {fds275747}
}

@article{fds275751,
   Author = {Faggin, BM and Zubieta, JK and Rezvani, AH and Cubeddu,
             LX},
   Title = {Neurotensin-induced dopamine release in vivo and in vitro
             from substantia nigra and nucleus caudate.},
   Journal = {The Journal of Pharmacology and Experimental
             Therapeutics},
   Volume = {252},
   Number = {2},
   Pages = {817-825},
   Year = {1990},
   Month = {February},
   ISSN = {0022-3565},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2138224},
   Keywords = {Animals • Caudate Nucleus • Dopamine •
             Electric Stimulation • Ergolines • Male •
             Neurotensin • Nomifensine • Potassium •
             Quinpirole • Rabbits • Rats • Rats, Inbred
             Strains • Receptors, Dopamine • Receptors,
             Dopamine D2 • Substantia Nigra • Sulpiride •
             drug effects • pharmacology • pharmacology* •
             secretion*},
   Abstract = {We compared the dopamine (DA) releasing effects of
             neurotensin (NT) from cell bodies (substantia nigra) and
             nerve terminals (nucleus caudate). In rats implanted with
             push-pull cannula, NT induced DA release from substantia
             nigra and nucleus caudate. NT was more potent in releasing
             DA from the substantia nigra than from the nucleus caudate
             (EC50%, 1.1 microM in substantia nigra and 9.8 microM in
             nucleus caudate). In vitro, in superfused rabbit brain
             slices, NT enhanced the depolarization-evoked release of DA
             and exerted a direct releasing effect. The latter was
             greater in the substantia nigra, and the former in the
             nucleus caudate. The direct releasing effect of NT was not
             inhibited, but enhanced by nomifensine (3 microM).
             Sulpiride, a D2 DA receptor antagonist, failed to modify
             NT-induced DA release; in addition, NT did not affect the
             inhibition of DA and acetylcholine release produced by
             LY-171555, a D2 DA agonist. In both the substantia nigra and
             the nucleus caudate, desensitization to the releasing effect
             of NT was observed, either after 2.5, 5, or 10 min of
             exposure to the peptide. A synergistic interaction on DA
             release was observed between NT and potassium (K+), and
             between NT and electrical stimulation. Greater synergism was
             observed with high extracellular K+. Pretreatment of
             striatal slices with 15 mM K+ produced a 9-fold enhancement
             of NT-induced DA release. When K+ (25 mM, 2 min) was given
             together with NT there was a 2- to 3-fold increase in DA
             release compared to the release evoked by K+ in the absence
             of NT.(ABSTRACT TRUNCATED AT 250 WORDS)},
   Language = {eng},
   Key = {fds275751}
}

@article{fds275605,
   Author = {Morrisett, RA and Rezvani, AH and Overstreet, D and Janowsky, DS and Wilson, WA and Swartzwelder, HS},
   Title = {MK-801 potently inhibits alcohol withdrawal seizures in
             rats.},
   Journal = {European Journal of Pharmacology},
   Volume = {176},
   Number = {1},
   Pages = {103-105},
   Year = {1990},
   Month = {January},
   ISSN = {0014-2999},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2155795},
   Keywords = {Acoustic Stimulation • Animals •
             Dibenzocycloheptenes • Diet • Dizocilpine Maleate
             • Ethanol • Male • Rats • Rats, Inbred
             Strains • Receptors, N-Methyl-D-Aspartate •
             Receptors, Neurotransmitter • Seizures • Substance
             Withdrawal Syndrome • adverse effects* •
             complications • etiology • pharmacology* •
             physiology* • prevention & control*},
   Abstract = {The ability of MK-801, an N-methyl-D-aspartate
             (NMDA)-channel antagonist, to suppress alcohol withdrawal
             seizures generated audio-genically was studied in adult male
             rats using a cross-over experimental design. MK-801
             treatment reduced overall seizure score and proportion of
             rats seizing. In comparison to other seizure models, alcohol
             withdrawal seizures seem to be particularly sensitive to
             MK-801, suggesting that mechanisms which result in seizure
             susceptibility after withdrawal of chronic ethanol exposure
             may be dependent upon sensitization or upregulation of NMDA
             processes.},
   Language = {eng},
   Key = {fds275605}
}

@article{fds275754,
   Author = {Rezvani, AH and Overstreet, DH and Janowsky, DS},
   Title = {Reduction in ethanol preference following injection of
             centrally and peripherally acting antimuscarinic
             agents.},
   Journal = {Alcohol and Alcoholism (Oxford, Oxfordshire)},
   Volume = {25},
   Number = {1},
   Pages = {3-7},
   Year = {1990},
   Month = {January},
   ISSN = {0735-0414},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2334493},
   Keywords = {Alcohol Drinking • Animals • Brain •
             Dose-Response Relationship, Drug • N-Methylscopolamine
             • Parasympatholytics • Rats • Rats, Inbred
             Strains • Receptors, Muscarinic • Scopolamine
             Derivatives • Scopolamine Hydrobromide • drug
             effects* • pharmacology • pharmacology*},
   Abstract = {Selectively bred alcohol-preferring (P) and alcohol
             non-preferring (NP) lines of rats were administered saline
             subcutaneously, and doses of 0.5 and 2.0 mg/kg of two
             antimuscarinic agents scopolamine (centrally acting) and
             methscopolamine (peripherally acting), twice daily
             respectively for a period of one day. Compared to saline,
             both doses of scopolamine and methscopolamine induced a
             significant reduction in ethanol consumption in the P line
             of rats, and both antimuscarinic agents significantly
             increased water intake. Thus, ethanol preference was
             dramatically reduced in these rats. In contrast, scopolamine
             had relatively little effect on either ethanol or water
             intake in the NP line of rats, while methscopolamine tended
             to suppress both ethanol and water intake. These findings
             suggest that peripheral muscarinic mechanisms may be
             involved in ethanol preference in P rats.},
   Language = {eng},
   Key = {fds275754}
}

@article{fds275606,
   Author = {Rezvani, AH and Janowsky, DS},
   Title = {Decreased alcohol consumption by verapamil in alcohol
             preferring rats.},
   Journal = {Progress in Neuro Psychopharmacology & Biological
             Psychiatry},
   Volume = {14},
   Number = {4},
   Pages = {623-631},
   Year = {1990},
   ISSN = {0278-5846},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2236588},
   Keywords = {Alcohol Drinking • Animals • Drinking •
             Eating • Injections, Subcutaneous • Male •
             Rats • Verapamil • drug effects •
             pharmacology* • psychology*},
   Abstract = {1. Calcium channel blockers have been proposed, in addition
             to inhibiting the influx of Ca++ into the cells, to possess
             a wide variety of pharmacological effects, including
             interference with certain neurotransmitters involved in
             mood, mental disorders and alcohol craving. Further, it has
             been documented that certain neurotransmitters are involved
             in alcohol craving both in animals and humans. 2. To
             investigate the effects of Ca(++)-channel antagonist on
             alcohol preference, verapamil in three doses (5, 10 and 15
             mg/kg) was injected (S.C.) twice daily over a period of one
             day in alcohol-preferring (P) and alcohol non-preferring
             (NP) rats at 9:00 a.m. and 4:00 p.m. 3. Water, alcohol and
             food intake were monitored. 4. Our results show that
             verapamil in doses of 10 and 15 mg/kg significantly (p less
             than 0.02 and 0.01, respectively) reduced the intake of
             ethanol and increased the intake of water by P rats.
             However, injection of an equal volume of saline did not
             change the pattern of alcohol intake. 5. These results
             suggest that a (++(+)-channel blocker such as verapamil,
             could, at least partially, attenuate alcohol preference in
             alcohol preferring rats. It is possible that verapamil
             exerts an inhibitory effect on alcohol preference by
             interfering with Ca++ channels, blocking serotonin uptake or
             through another mechanism(s).},
   Language = {eng},
   Key = {fds275606}
}

@article{fds275749,
   Author = {Overstreet, DH and Rezvani, AH and Janowsky, DS},
   Title = {Increased hypothermic responses to ethanol in rats
             selectively bred for cholinergic supersensitivity.},
   Journal = {Alcohol and Alcoholism (Oxford, Oxfordshire)},
   Volume = {25},
   Number = {1},
   Pages = {59-65},
   Year = {1990},
   ISSN = {0735-0414},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2334497},
   Keywords = {Alcoholic Intoxication • Animals • Body
             Temperature Regulation • Brain • Ethanol •
             Exploratory Behavior • Male • Motor Activity
             • Postural Balance • Rats • Rats, Inbred
             Strains • Receptors, Cholinergic • Selection,
             Genetic • Sleep Stages • drug effects • drug
             effects* • genetics • pharmacokinetics •
             pharmacology*},
   Abstract = {The behavioral and hypothermic effects of ethanol were
             studied in the Flinders Sensitive Line (FSL) and Flinders
             Resistant Line (FRL) rats, selectively bred for differences
             in cholinergic sensitivity. The FSL hypercholinergic rats
             exhibited a significantly greater degree of hypothermia than
             the FRL rats, or a group of weight-matched randomly bred
             rats. Although there were some trends for the FSL rats to
             appear more depressed behaviorally after receiving ethanol,
             there were no significant differences between the FSL and
             FRL rats on quantitative behavioral measures. Blood ethanol
             concentrations were slightly lower in the FRL rats, but
             there were no differences between the FSL and control rats.
             These findings suggest an association between cholinergic
             mechanisms and ethanol sensitivity with regard to body
             temperature effect, but a direct causal relationship cannot
             be established because of similar differential sensitivities
             of FSL and FRL rats to a range of other neurotransmitter-altering
             drugs on this parameter.},
   Language = {eng},
   Key = {fds275749}
}

@article{fds275750,
   Author = {Rezvani, AH and Mack, CM and De Lacy and PA and Janowsky,
             DS},
   Title = {Verapamil effects on physiological and behavioral responses
             to ethanol in the rat.},
   Journal = {Alcohol and Alcoholism (Oxford, Oxfordshire)},
   Volume = {25},
   Number = {1},
   Pages = {51-58},
   Year = {1990},
   ISSN = {0735-0414},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2334496},
   Keywords = {Alcoholic Intoxication • Animals • Body
             Temperature Regulation • Brain • Ethanol •
             Female • Injections, Intraventricular • Male
             • Motor Skills • Rats • Rats, Inbred Strains
             • Verapamil • drug effects • drug effects*
             • pharmacology* • psychology*},
   Abstract = {Experiments were performed to determine the ability of
             verapamil to reverse ethanol-induced hypothermia and
             behavioral changes. Permanent cannulae for
             intracerebroventricular (i.c.v.) infusion were implanted
             bilaterally in rats following standard stereotaxic
             procedures. Following post-operative recovery, either
             verapamil or artificial cerebral spinal fluid (ACSF) was
             infused i.c.v., followed by 4.0 g/kg ethanol in saline
             administered by intragastric gavage. Changes in body
             temperature and overall activity were monitored. In another
             series of experiments, rats were given either i.c.v.
             verapamil or ACSF followed by 1.5 g/kg intraperitoneal
             ethanol. Ability to turn over and open-field activity were
             monitored. In addition, to investigate the action of
             verapamil alone on body temperature, rats were infused
             i.c.v. either with verapamil or control ACSF, followed by
             intragastric administration of a volume of saline equal to
             4.0 g/kg ethanol (20% v/v). At an ambient temperature of 22
             degrees C, verapamil, infused prior to ethanol
             administration, significantly and rapidly attenuated the
             thermolytic action of ethanol. Central administration of
             verapamil alone did not induce a significant change in body
             temperature until more than 1.5 hr after injection, at which
             time temperature began to gradually increase. Pretreatment
             with verapamil induced significantly faster recovery from
             ethanol-induced changes in overall activity. Only a
             non-significant reversal of ethanol's effects on open-field
             activity and time taken to turn over occurred. These results
             demonstrate that verapamil can significantly antagonize
             ethanol-induced hypothermia and possibly motor disturbances
             in rats, leading us to postulate the possible involvement of
             neuronal Ca2+ channels in these effects of
             ethanol.},
   Language = {eng},
   Key = {fds275750}
}

@article{fds275752,
   Author = {Pucilowski, O and Eichelman, B and Overstreet, DH and Rezvani, AH and Janowsky, DS},
   Title = {Enhanced affective aggression in genetically bred
             hypercholinergic rats.},
   Journal = {Neuropsychobiology},
   Volume = {24},
   Number = {1},
   Pages = {37-41},
   Year = {1990},
   ISSN = {0302-282X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2132639},
   Abstract = {Affective aggression was studied in pairs of Flinders
             Sensitive Line hypercholinergic rats (FSL) and Flinders
             Resistant Line (FRL) rats in shock-induced and
             apomorphine-induced fighting tests. FSL rats were
             significantly more aggressive in both tests. They had higher
             pain threshold, assessed by the jump-flinch method, than FRL
             rats. It is concluded that genetically developed cholinergic
             system supersensitivity has resulted in enhanced
             responsiveness to stimuli eliciting affective
             aggression.},
   Doi = {10.1159/000119040},
   Key = {fds275752}
}

@article{fds275753,
   Author = {Rezvani, AH and Overstreet, DH and Janowsky, DS},
   Title = {Genetic serotonin deficiency and alcohol preference in the
             fawn hooded rats.},
   Journal = {Alcohol and Alcoholism (Oxford, Oxfordshire)},
   Volume = {25},
   Number = {5},
   Pages = {573-575},
   Year = {1990},
   ISSN = {0735-0414},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2088356},
   Keywords = {Alcohol Drinking • Alcoholism • Animals •
             Brain • Fluoxetine • Rats • Rats, Inbred
             Strains • Receptors, Serotonin • Serotonin •
             deficiency* • drug effects • genetics* •
             metabolism • pharmacology},
   Language = {eng},
   Key = {fds275753}
}

@article{fds275755,
   Author = {Overstreet, DH and Dilsaver, SC and Rezvani, AH and Janowsky,
             DS},
   Title = {Selective antagonistic effects of exposure to bright light
             on the hypothermic action of ethanol.},
   Journal = {Alcohol and Alcoholism (Oxford, Oxfordshire)},
   Volume = {25},
   Number = {6},
   Pages = {661-665},
   Year = {1990},
   ISSN = {0735-0414},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2085349},
   Keywords = {Alcoholic Intoxication • Animals • Body
             Temperature Regulation • Ethanol • Hypothalamus
             • Phototherapy* • Postural Balance • Rats
             • Rats, Inbred Strains • drug effects • drug
             effects* • pharmacology* • physiopathology},
   Abstract = {Flinders Sensitive and Resistant Lines of rats, which are
             differentially sensitive to the hypothermic effects of both
             muscarinic agonists and ethanol, were exposed to full
             spectrum artificial bright light for eight days, because
             exposure to bright light has been shown to blunt hypothermic
             responses to muscarinic agonists. There was a selective
             blunting of the hypothermic effects of ethanol, but no
             significant change in the intoxicating effects of ethanol,
             as measured by evaluation of the righting reflex. The
             selective effect of exposure to bright light on the
             hypothermic actions of ethanol suggests that bright light
             may be modifying the function of only a limited number of
             brain regions, including the hypothalamus.},
   Language = {eng},
   Key = {fds275755}
}

@article{fds275745,
   Author = {Kawakami, M and Meyer, AA and Johnson, MC and Rezvani,
             AH},
   Title = {Immunologic consequences of acute ethanol ingestion in
             rats.},
   Journal = {Journal of Surgical Research},
   Volume = {47},
   Number = {5},
   Pages = {412-417},
   Year = {1989},
   Month = {November},
   ISSN = {0022-4804},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2554061},
   Keywords = {Alcoholic Intoxication • Animals • Chemotaxis,
             Leukocyte • Concanavalin A • DNA • Immunity*
             • Leukocyte Count • Lipopolysaccharides •
             Lymphocytes • Male • N-Formylmethionine
             Leucyl-Phenylalanine • Neutrophils • Peroxidase
             • Rats • Rats, Inbred Strains • Spleen •
             biosynthesis • cytology • immunology •
             immunology* • metabolism • pharmacology},
   Abstract = {Acute ethanol (EtOH) intoxication is commonly associated
             with many medical and surgical problems which primarily or
             secondarily involve infection. Chronic EtOH ingestion has
             been associated with immune dysfunction and an increased
             risk of infection; however, the relationship of acute EtOH
             exposure and immune function has not been clearly defined.
             To determine if there is a relationship between acute EtOH
             intoxication and immune function, the effects of a single
             EtOH ingestion on immune function were studied in a rat
             model. Acute intoxication was produced by gavage feeding of
             3 g/kg of EtOH, and immune function was evaluated by in vivo
             chemotaxis to a chemotactic peptide, N-formyl-methionyl-leucyl-phenylalanine
             and responsiveness of splenic lymphocytes to B- and T-cell
             mitogens. Chemotaxis was significantly suppressed at 4 hr
             (49.0 +/- 5.1% of control) after EtOH ingestion (P = 0.001),
             but returned to normal by 24 hr and remained at that level.
             However, acute EtOH ingestion showed no suppressive effects
             on lymphocyte responsiveness to either concanavalin A or
             LPS. These results indicate that a single ingestion of EtOH
             has the potential to transiently suppress chemotactic
             function of granulocytes but not affect lymphocyte mitogenic
             responsiveness in rats. This potential may contribute to
             increased susceptibility to infection in patients after EtOH
             ingestion.},
   Language = {eng},
   Key = {fds275745}
}

@article{fds275746,
   Author = {Rezvani, AI and Collins, DM and Sena, AC},
   Title = {Measurement of extracellular calcium ions within the
             hypothalamus of the freely-moving cat: A novel
             approach},
   Journal = {Journal of Liquid Chromatography},
   Volume = {12},
   Number = {8},
   Pages = {1323-1332},
   Publisher = {Informa UK Limited},
   Year = {1989},
   Month = {June},
   url = {http://dx.doi.org/10.1080/01483918908049509},
   Abstract = {In order to investigate the kinetics of calcium ion (Ca++)
             activity within the hypothalamus by high performance liquid
             chromatography, standard push-pull guide cannulae were
             implanted stereotaxically above the hypothalamus of the cat.
             Following post-operative recovery, an isotonic artificial
             cerebrospinal fluid (ACSF) was perfused in the site at a
             rate of 25 ul/min over successive intervals of 5.0 min. In
             the mid-point of a sequence of repeated push-pull
             perfusions, verapamil (4.0 ug/ul) was added to the
             perfusate. Samples collected from the hypothalamus of the
             freely-moving cat were analyzed for calcium concentration by
             an HPLC conductivity detector. The results showed that
             verapamil perfused within the hypothalamus of the cat caused
             an efflux of calcium ion into the perfusate which was
             detected by HPLC. This study proposes a new approach to
             precisely determine the calcium concentration in
             extracellular fluid in awake freely-moving animals. © 1989,
             Taylor & Francis Group, LLC. All rights reserved.},
   Doi = {10.1080/01483918908049509},
   Key = {fds275746}
}

@article{fds275743,
   Author = {Overstreet, DH and Janowsky, DS and Rezvani, AH},
   Title = {Alcoholism and depressive disorders: is cholinergic
             sensitivity a biological marker?},
   Journal = {Alcohol and Alcoholism (Oxford, Oxfordshire)},
   Volume = {24},
   Number = {3},
   Pages = {253-255},
   Year = {1989},
   ISSN = {0735-0414},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2757700},
   Keywords = {Acetylcholine • Alcoholism • Arousal • Body
             Temperature Regulation • Brain • Cholinergic
             Fibers • Depressive Disorder • Evoked Potentials,
             Auditory • Humans • Physostigmine • Reaction
             Time • Receptors, Cholinergic • Sleep, REM •
             diagnosis • diagnostic use • drug effects •
             physiology • physiology* • physiopathology*},
   Abstract = {There is an overlap between alcoholism and depressive
             disorders. However, alcoholics tend to be resistant to the
             effect of cholinergic agonists, whereas depressives tend to
             be more sensitive. A recently developed animal model of
             depression which is more sensitive to cholinergic agonists
             is also more sensitive to the acute effects of ethanol.
             These consistent human and animal studies suggest that
             cholinergic challenges may be helpful in separating
             alcoholics from depressives.},
   Language = {eng},
   Key = {fds275743}
}

@article{fds275744,
   Author = {Carl, PL and Cubeddu, LX and Lindley, C and Myers, RD and Rezvani,
             AH},
   Title = {Do humoral factors mediate cancer chemotherapy-induced
             emesis?},
   Journal = {Drug Metabolism Reviews (Informa)},
   Volume = {21},
   Number = {2},
   Pages = {319-333},
   Year = {1989},
   ISSN = {0360-2532},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2699850},
   Keywords = {Animals • Antineoplastic Agents • Cats • Dogs
             • Humans • Lymphokines • Rats • Vomiting
             • adverse effects* • chemically induced* •
             pharmacology*},
   Language = {eng},
   Doi = {10.3109/03602538909029944},
   Key = {fds275744}
}

@article{fds275742,
   Author = {Gordon, CJ and Mohler, FS and Watkinson, WP and Rezvani,
             AH},
   Title = {Temperature regulation in laboratory mammals following acute
             toxic insult.},
   Journal = {Toxicology},
   Volume = {53},
   Number = {2-3},
   Pages = {161-178},
   Year = {1988},
   Month = {December},
   ISSN = {0300-483X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/3062847},
   Keywords = {Animals • Animals, Laboratory* • Body Temperature
             Regulation • Cricetinae • Guinea Pigs • Mice
             • Poisoning* • Rabbits • Rats • drug
             effects* • physiopathology},
   Abstract = {The purpose of this paper is to provide a concise review of
             the effects of acute chemical toxicity on thermoregulation
             in mammals, with particular emphasis on the effects of
             xenobiotic compounds in laboratory rodents. It has been
             shown that acute administration of compounds such as nickel,
             cadmium, lead, and some pesticides causes a reduction in the
             body temperature of mice when tested at normal room
             temperatures. When provided with the option of selecting
             their preferred ambient temperature, the toxic-treated
             animals generally select cool temperatures which augment the
             hypothermic effect of the toxic compounds. It would appear
             that many of the xenobiotic compounds have central as well
             as peripheral effects on the control of body temperature.
             That is, the hypothermic animals select cool temperatures, a
             condition indicative of a centrally mediated decrease in the
             set-point. This decrease in set-point, or regulated
             hypothermia, may be beneficial to survival since the
             lethality of most xenobiotic compounds increases with rising
             body temperature. The observation that acute doses of
             various compounds leads to behaviorally and autonomically
             mediated changes in body temperature may have significant
             implications for the measurement of other biological effects
             of these chemical agents (e.g., CNS dysfunction,
             bradycardia, immunosuppression).},
   Language = {eng},
   Key = {fds275742}
}

@article{fds275741,
   Author = {Gordon, CJ and Fogelson, L and Mohler, F and Stead, AG and Rezvani,
             AH},
   Title = {Behavioral thermoregulation in the rat following the oral
             administration of ethanol.},
   Journal = {Alcohol and Alcoholism (Oxford, Oxfordshire)},
   Volume = {23},
   Number = {5},
   Pages = {383-390},
   Year = {1988},
   ISSN = {0735-0414},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/3228459},
   Keywords = {Adaptation, Physiological • Administration, Oral •
             Adult • Animals • Body Temperature • Body
             Temperature Regulation • Ethanol • Humans •
             Male • Rats • Rats, Inbred F344 •
             administration & dosage • drug effects* •
             pharmacology},
   Abstract = {To assess if ethyl alcohol (ethanol) causes a reduction in
             the set-point for control of body temperature, behavioral
             thermoregulatory responses in the Fischer rat were measured
             following a single oral administration of ethanol. In a
             preliminary study, five rats were given 3.0 g/kg ethanol
             dissolved in saline (20%; v/v) by gavage and placed in a
             longitudinal temperature gradient for 2 hr. The temperature
             gradient permitted the rats to behaviorally thermoregulate
             (i.e. select a thermal preferendum). The selected ambient
             temperature (Ta) in the temperature gradient was notably
             lower during the initial and final stages of the test period
             when compared to the response of rats administered similar
             volumes of saline. Colonic temperature upon removal from the
             gradient was approximately 1.0 degree C below that of the
             saline-treated animals. In a follow-up study, rats were
             placed in the temperature gradient for 1 hr for
             accommodation purposes. The rats were then gavaged with 0,
             1.0 or 3.0 g/kg ethanol and placed back in the gradient for
             another 2 hr. Selected Ta was significantly reduced in the
             3.0 g/kg group during the second hour post-ethanol exposure.
             The 1.0 g/kg dosage had little effect on selected Ta. As in
             the preliminary study, the colonic temperature of the rats
             in the follow up study given 3.0 g/kg was 1.0 degree C below
             that of the control at 2 hr post-injection. Because the 3.0
             g/kg treated animals were significantly hypothermic and
             selected cooler Tas in the temperature gradient, it was
             concluded that ethanol exerted a lowering of the set-point
             for control of body temperature.},
   Language = {eng},
   Key = {fds275741}
}

@article{fds275740,
   Author = {Beleslin, DB and Rezvani, AH and Myers, RD},
   Title = {Rostral hypothalamus: a new neuroanatomical site of
             neurochemically-induced emesis in the cat.},
   Journal = {Brain Research Bulletin},
   Volume = {19},
   Number = {2},
   Pages = {239-244},
   Year = {1987},
   Month = {August},
   ISSN = {0361-9230},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2889512},
   Keywords = {Adrenergic alpha-Antagonists • Animals • Cats
             • Clonidine • Female • Hypothalamus •
             Hypothermia • Norepinephrine • Vomiting •
             anatomy & histology • antagonists & inhibitors •
             chemically induced • chemically induced* •
             metabolism • pharmacology • physiology* •
             prevention & control},
   Abstract = {The localized effect of noradrenergic agonists administered
             directly in the anterior hypothalamic preoptic area (AH/POA)
             in inducing emesis in the cat was investigated. Of the
             noradrenergic agonists tested, which included
             norepinephrine, clonidine, phenylephrine and methoxamine,
             only clonidine in doses of 5.0-50.0 micrograms was found to
             evoke emesis consistently when micro-injected in a volume of
             1.0 microliter into AH/POA of the unrestrained cat. The
             emetic response to clonidine was short-lasting, generally
             dose-dependent in terms of latency and frequency, and
             occurred in bouts of one to three episodes. The sequence of
             the vomiting response, beginning with licking and retching,
             functionally resembled a normal pattern of an emetic
             response. The clonidine-induced emesis was not antagonized
             by the following antagonists micro-injected in AH/POA just
             prior to clonidine: alpha-adrenergic blocking agents,
             yohimbine, RX 781094 and phentolamine; the antimuscarinic
             drug, atropine; the serotonin antagonist, methysergide; the
             opioid antagonist, naloxone; and the dopamine antagonist,
             chlorpromazine. Therefore, it would appear that
             clonidine-induced emesis is not mediated by alpha
             noradrenergic, serotonergic, dopaminergic, muscarinic and
             opiate receptor systems within the AH/POA of the cat.
             Finally, the obtained results show that apart from the area
             postrema and a circumscribed zone of the brain-stem
             reticular formation, the hypothalamus is now implicated as a
             neuroanatomical site in the central nervous system mechanism
             underlying neurochemically-induced emesis.},
   Language = {eng},
   Key = {fds275740}
}

@article{fds275738,
   Author = {Myers, RD and Beleslin, DB and Rezvani, AH},
   Title = {Hypothermia: role of alpha 1- and alpha 2-noradrenergic
             receptors in the hypothalamus of the cat.},
   Journal = {Pharmacology, Biochemistry, and Behavior},
   Volume = {26},
   Number = {2},
   Pages = {373-379},
   Year = {1987},
   Month = {February},
   ISSN = {0091-3057},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/3033698},
   Keywords = {Animals • Body Temperature • Cats • Clonidine
             • Female • Hypothermia • Kinetics •
             Methoxamine • Norepinephrine • Phenylephrine
             • Receptors, Adrenergic • drug effects •
             pharmacology • pharmacology* • physiology* •
             physiopathology*},
   Abstract = {The purpose of this study was to characterize the alpha 1-
             and alpha 2-noradrenergic receptor sub-types which could
             mediate the hypothermic response produced by norepinephrine
             (NE) and other alpha-noradrenergic agonists applied to the
             thermosensitive zone of the hypothalamus. An array of four
             guide tubes was implanted stereotaxically so that their tips
             rested just above the anterior hypothalamic, preoptic area
             (AH/POA) of the cat. Following post-operative recovery, a
             micro-injection of an agonist or antagonist of NE receptors
             or control CSF vehicle was given in a volume of 1.0-2.0
             microliter in the AH/POA in each of the unrestrained cats.
             The alpha 1-noradrenergic receptor agonist, phenylephrine,
             but not methoxamine, applied to the AH/POA produced a
             dose-dependent hypothermia of up to 2.0 degrees C. When
             applied similarly, the alpha 2-noradrenergic agonist
             clonidine, as well as norepinephrine, which acts on both
             alpha 1- and alpha 2-noradrenergic receptors, also induced a
             decline in the cat's core temperature of up to 1.5 degrees
             C. The hypothermic response of clonidine was inhibited by
             pre-treatment of the AH/POA with a micro-injection of the
             selective alpha 2-noradrenergic blocking agent, yohimbine.
             However, yohimbine given similarly in the cat's AH/POA
             potentiated significantly both the phenylephrine and
             norepinephrine-induced hypothermia. The combined alpha 1-,
             alpha 2-noradrenergic receptor antagonist, phentolamine,
             also injected into AH/POA inhibited the thermolytic response
             evoked by both phenylephrine and norepinephrine, whereas it
             was virtually ineffective against the clonidine-induced
             hypothermia. These results, therefore, strongly suggest that
             both alpha 1- and alpha 2-noradrenergic receptors subserve
             the coordinated thermoregulatory mechanisms in AH/POA which
             are required for the functional dissipation of body heat and
             the consequent evocation of hypothermia.},
   Language = {eng},
   Key = {fds275738}
}

@article{fds275734,
   Author = {Rezvani, AH and Denbow, DM and Myers, RD},
   Title = {α-Melanocyte-stimulating hormone (α-MSH) release from
             perifused rat hypothalamic slices},
   Journal = {Brain Research},
   Volume = {413},
   Number = {2},
   Pages = {259-266},
   Publisher = {Elsevier BV},
   Year = {1987},
   Month = {January},
   ISSN = {0361-9230},
   url = {http://dx.doi.org/10.1016/0361-9230(86)90017-1},
   Keywords = {Animals • Anti-Inflammatory Agents, Non-Steroidal
             • Body Temperature • Cats • Dose-Response
             Relationship, Drug • Drug Synergism • Endotoxins*
             • Escherichia coli • Female • Fever •
             Injections, Intraventricular • Melanocyte-Stimulating
             Hormones • Stereotaxic Techniques • Time Factors
             • administration & dosage • administration &
             dosage* • drug effects* • etiology •
             physiopathology*},
   Abstract = {A perifusion sytem was developed to investigate the control
             of α-melanocyte-stimulating hormone (α-MSH) release from
             rat brain. Hypothalamic slices were perifused with
             Krebs-Ringer bicarbonate (KRB) medium supplemented with
             glucose, bacitracin and bovine serum albumine. Fractions
             were set apart every 3 min and α-MSH levels were measured
             by means of a specific and sensitive radioimmunoassay
             method. Hypothalamic tissue in normal KRB medium released
             α-MSH at a constant rate corresponding to 0.1% of the total
             hypothalamic content per 3 min. The basal release was not
             altered by Ca2+ omission in the medium or addition of the
             sodium channel blocker tetrodotoxine (TTX). Depolarizing
             agents such as potassium (50mM) and veratridine (50 μM),
             which is known to increase Na+ conductance, significantly
             stimulated α-MSH release in a Ca2+ -dependent manner. When
             Na+-channels were blocked by TTX (0.5 μM) the stimulatory
             effect of veratridine was completely abolished whereas the
             K+-evoked release was unaffected. These findings suggest
             that: (1) voltage-dependent sodium channels are present on
             α-MSH hypothalamic neurons; (2) depolarization by K+
             induces a marked stimulation of α-MSH release; (3) K+-and
             veratridine-evoked releases are calcium-dependent.
             Altogether, these data provide evidence for a
             neurotransmitter or neuromodulator role for α-MSH in rat
             hypothalamus.},
   Language = {eng},
   Doi = {10.1016/0361-9230(86)90017-1},
   Key = {fds275734}
}

@article{fds275737,
   Author = {Lee, TF and Rezvani, AH and Hepler, JR and Myers,
             RD},
   Title = {Neurotensin releases norepinephrine differentially from
             perfused hypothalamus of sated and fasted
             rat},
   Journal = {American Journal of Physiology. Endocrinology and
             Metabolism},
   Volume = {252},
   Number = {1},
   Pages = {15/1},
   Year = {1987},
   Month = {January},
   ISSN = {0002-9513},
   Keywords = {Animals • Eating • Fasting • Female •
             Hypothalamus • Kinetics • Male • Neurotensin
             • Norepinephrine • Organ Specificity •
             Perfusion • Rats • Rats, Inbred Strains •
             Stereotaxic Techniques • drug effects •
             pharmacology* • physiology* • secretion •
             secretion*},
   Abstract = {The central injection of neurotensin (NT) has been reported
             to attenuate the intake of food in the fasted animal. To
             determine whether endogenous norepinephrine (NE) is involved
             in the satiating effect of NT, the in vivo activity of NE in
             circumscribed sites in the hypothalamus of the
             unanesthetized rat was examined. Bilateral guide tubes for
             push-pull perfusion were implanted stereotaxically to rest
             permanently above one of several intended sites of
             perfusion, which included the paraventricular nucleus (PVN),
             ventromedial nucleus (VMN), and the lateral hypothalamic
             (LH) area. After endogenous stores of NE at a specific
             hypothalamic locus were radiolabeled by microinjection of
             0.02-0.5 μCi of [3H]NE, an artificial cerebrospinal fluid
             was perfused at the site at a rate of 20 μl/min over
             successive intervals of 5.0 min. When 0.05 or 0.1 μg/μl NT
             (0.03-0.6 mM) was added to the perfusate, the peptide served
             either to enhance or reduce the local release of NE at 50%
             of the sites of perfusion. In these experiments, the
             circumscribed effect of NT on the characteristics of
             catecholamine efflux depended entirely on the state of
             hunger or satiety of the rat. That is, when NT was perfused
             in the fully satiated rat, NE release was augmented within
             the PVN or VMN; conversely, NE release was inhibited in the
             LH. In the animal fasted for 18-22 h, NT exerted an opposite
             effect on the activity of NE within the same anatomical loci
             in that the efflux of NE was enhanced in the LH but
             attenuated or unaffected in the PVN or VMN. Taken together,
             these obervations provide experimental support for the
             viewpoint that NT could act as a neuromodulator of the
             activity of hypothalamic noradrenergic neurons that are
             thought to play a functional role in the regulation of food
             intake.},
   Language = {eng},
   Key = {fds275737}
}

@article{fds275739,
   Author = {Rezvani, AH and McManus, KT and Myers, RD},
   Title = {Rate of in vivo verapamil exchange within the hypothalamus
             of the cat as examined by push-pull perfusion.},
   Journal = {Neurochemical Research},
   Volume = {11},
   Number = {12},
   Pages = {1643-1651},
   Year = {1986},
   Month = {December},
   ISSN = {0364-3190},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/3822047},
   Keywords = {Animals • Cats • Hypothalamus • Verapamil
             • metabolism*},
   Abstract = {To investigate the characteristics of the uptake within
             hypothalamic tissue of the Ca2+-channel blocker, verapamil,
             push-pull canulae were implanted bilaterally above the
             anterior hypothalamic-preoptic area (AH/POA) and posterior
             hypothalamus (PH) of the cat. The functional reactivity of
             these two anatomical regions was verified in the
             unrestrained cat, prior to a push-pull perfusion, by a
             micro-injection of either 5-7 micrograms norepinephrine (NE)
             into AH/POA, or by perfusion of 50 mM Ca2+ within the PH,
             both of which induce a transient decline in the cat's core
             temperature. Verapamil was perfused in a concentration of
             0.4, 2.0 or 4.0 micrograms/microliter for successive 10 and
             20 min intervals within these NE and Ca2+-sensitive sites. A
             quantitative analysis of verapamil in each sample of
             perfusate was performed double-blind by HPLC-spectrophotometric
             detection. The results showed that the percent recovery of
             verapamil after the 10 min interval was always less than
             that after the next 20 min period of perfusion. These
             recovery values were independent of the site of perfusion
             and the concentration of verapamil. However, the mean uptake
             of verapamil into tissue after 10 min was significantly
             greater than that after the 20 min period for all
             concentrations tested. These results demonstrate that the
             hypothalamus has a time-dependent characteristic to
             incorporate a Ca2+-channel blocker into the parenchyma. Once
             the point of tissue saturation is reached, a steady-state
             level of verapamil uptake is established.},
   Language = {eng},
   Key = {fds275739}
}

@article{fds275732,
   Author = {Beleslin, DB and Rezvani, AH and Myers, RD},
   Title = {Dissociation of locomotor impairment from mydriasis evoked
             by clonidine injected into cat's rostral
             hypothalamus.},
   Journal = {Brain Research Bulletin},
   Volume = {17},
   Number = {3},
   Pages = {379-385},
   Year = {1986},
   Month = {September},
   ISSN = {0361-9230},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2876757},
   Keywords = {Adrenergic alpha-Agonists • Adrenergic
             alpha-Antagonists • Animals • Cats •
             Clonidine • Female • Injections • Motor
             Activity • Phentolamine • Preoptic Area •
             Pupil • Receptors, Adrenergic, alpha • Sleep
             • Yohimbine • drug effects* • pharmacology
             • pharmacology*},
   Abstract = {The anterior hypothalamic preoptic area (AH/POA) was
             examined as a possible site of action of clonidine and other
             alpha noradrenergic receptor agonists which evoke motor and
             autonomic changes. Chronically indwelling guide cannulae
             were implanted stereotaxically in the diencephalon of the
             cat. Following post-operative recovery, a micro-injection
             into AH/POA was made in a volume of 1.0 microliter of one of
             the following compounds: 5.0-50.0 micrograms clonidine,
             5.0-50.0 micrograms norepinephrine, 5.0-50.0 micrograms
             phenylephrine and 5.0-50.0 micrograms methoxamine. The
             smallest dose of 5.0 micrograms clonidine produced a brief
             period of restlessness, licking, retching and emesis but a
             much longer-lasting mydriasis. When the dose of clonidine
             was raised to 20 micrograms, the cat became behaviorally
             sedated, after a latency of about 15 min, for a period of up
             to 1.0-2.0 hr. This was accompanied by a prolonged period of
             mydriasis and preceded by a short interval of restlessness,
             licking, retching and emesis. After the highest dose of 50.0
             micrograms clonidine was micro-injected in AH/POA, a
             profound impairment of motor activity, adynomia and
             restlessness developed within 15-20 min, persisted for 30 to
             60 min and was accompanied also by mydriasis with maximal
             pupillary dilation lasting for up to six hr. When 5.0-50.0
             micrograms phenylephrine or 5.0-50.0 micrograms
             norepinephrine were micro-injected at clonidine-reactive
             sites in AH/POA, only rarely were brief instances of
             restlessness, licking, retching and emesis observed;
             however, methoxamine at all doses tested failed to produce
             any visible signs of autonomic or motor disturbance.(ABSTRACT
             TRUNCATED AT 250 WORDS)},
   Language = {eng},
   Key = {fds275732}
}

@article{fds275735,
   Author = {Rezvani, AH and Beleslin, DB and Myers, RD},
   Title = {Neuroanatomical mapping of hypothalamic regions mediating
             verapamil hyper- and hypothermia in the cat.},
   Journal = {Brain Research Bulletin},
   Volume = {17},
   Number = {2},
   Pages = {249-254},
   Year = {1986},
   Month = {August},
   ISSN = {0361-9230},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/3768734},
   Keywords = {Animals • Body Temperature • Body Temperature
             Regulation • Cats • Colon • Hypothalamus
             • Verapamil • administration & dosage •
             anatomy & histology* • drug effects • drug
             effects* • pharmacology* • physiology*},
   Abstract = {Guide cannulae for microinjection and push-pull perfusion in
             the unrestrained cat were implanted bilaterally in the
             anterior hypothalamic, preoptic area (AH/POA) and posterior
             hypothalamus (PH). Postoperatively, the region was first
             identified in AH/POA which was reactive to norepinephrine or
             in PH to excess Ca++ ions; in both cases a hypothermic
             response was produced. Then either an artificial CSF control
             vehicle or the Ca++ ion channel blocking agent, verapamil,
             was perfused for 30 min by means of push-pull cannulae at a
             rate of 25.0 microliters/min. Verapamil 0.4, 2.0 and 4.0
             micrograms/microliter) induced a concentration-dependent
             hypothermia when perfused within AH/POA sites but
             hyperthermia when perfused in the caudal hypothalamus. An
             anatomical analysis of the sites of perfusion revealed that
             verapamil's thermolytic effect was localized within the
             classical thermosensitive region of the cat's diencephalon,
             a region ventral to the anterior commissure and dorsal to
             the optic chiasm. On the other hand, the loci in which
             verapamil evoked thermogenesis were localized to a region
             dorsal to the mammillary bodies and caudal to the descending
             columns of the fornix. It is suggested that verapamil
             interferes with Ca++ ion channels in the PH to shift the
             cat's "set-point" temperature. Conversely, however,
             verapamil apparently could act on catecholaminergic
             terminals in AH/POA to enhance the presynaptic release of
             norepinephrine which, in turn, stimulates the heat loss
             pathway to yield hypothermia.},
   Language = {eng},
   Key = {fds275735}
}

@article{fds275733,
   Author = {Rezvani, AH and Mack, CM and Crovi, SI and Myers,
             RD},
   Title = {Central Ca++-channel blockade reverses ethanol-induced
             poikilothermia in the rat.},
   Journal = {Alcohol},
   Volume = {3},
   Number = {4},
   Pages = {273-279},
   Year = {1986},
   Month = {July},
   ISSN = {0741-8329},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/3755956},
   Keywords = {Animals • Body Temperature Regulation • Brain
             • Calcium • Cell Membrane Permeability •
             Ethanol • Female • Injections, Intraventricular
             • Rats • Rats, Inbred Strains • Verapamil
             • antagonists & inhibitors • drug effects •
             drug effects* • metabolism* • pharmacology •
             pharmacology*},
   Abstract = {Two series of experiments were performed to determine the
             possible involvement of Ca++ channels in the thermolytic
             action of ethanol administered at a room temperature of 22
             degrees C. In one group of 11 adult female Sprague-Dawley
             rats, stainless steel guide cannulae were implanted
             stereotaxically above the lateral cerebral ventricle. Prior
             to an experiment, a thermistor probe was inserted into the
             colon so that core temperature could be monitored
             continuously for up to six hours or until the temperature
             had returned to a previous baseline level. When the animal's
             body temperature had stabilized, a dose of 4.0 g/kg in a v/v
             solution of 20% ethanol was given by intragastric gavage.
             After the body temperature had declined by about 2.0 degrees
             C, ordinarily 30 min after ethanol administration, either
             control CSF or the vehicle plus one of four doses of
             verapamil (8.3, 25, 50 and 100 micrograms) was infused
             intracerebroventricularly (ICV) in a volume of 10
             microliter. In a second group of 7 unoperated rats, either
             4.0 g/kg ethanol or a physiological saline control solution
             was administered isovolumetrically by intragastric gavage;
             then, 30 min later, either 3.0 or 10.0 mg/kg verapamil was
             injected intraperitoneally. At an ambient temperature of 22
             degrees C, ethanol gavage produced a significant decline in
             colonic temperature which was unaffected by physiological
             saline given by the same route. Although the CSF control
             vehicle was without effect, verapamil administered ICV
             attenuated the thermolytic action of ethanol in all doses
             tested; however, the lowest dose exerted its antagonist
             effect but with a longer latency. Conversely, when verapamil
             was given systemically, the hypothermic action of ethanol
             was significantly potentiated in a dose-dependent
             manner.(ABSTRACT TRUNCATED AT 250 WORDS)},
   Language = {eng},
   Key = {fds275733}
}

@article{fds275736,
   Author = {REZVANI, AH and HUTTUNEN, P and MYERS, RD},
   Title = {Effect of Morphine and Ethanol on Neuronal Release of
             Norepinephrine from the Hypothalamus: Relation to Body
             Temperature},
   Journal = {Annals of the New York Academy of Sciences},
   Volume = {473},
   Number = {1},
   Pages = {516-519},
   Publisher = {WILEY},
   Year = {1986},
   Month = {January},
   url = {http://dx.doi.org/10.1111/j.1749-6632.1986.tb23647.x},
   Doi = {10.1111/j.1749-6632.1986.tb23647.x},
   Key = {fds275736}
}

@article{fds275730,
   Author = {Beleslin, DB and Rezvani, AH and Myers, RD},
   Title = {Divergent action of verapamil perfused in two hypothalamic
             areas on body temperature of the cat.},
   Journal = {Neuroscience Letters},
   Volume = {57},
   Number = {3},
   Pages = {307-312},
   Year = {1985},
   Month = {June},
   ISSN = {0304-3940},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/4034099},
   Keywords = {Animals • Body Temperature • Cats •
             Hypothalamus • Hypothalamus, Posterior • Preoptic
             Area • Verapamil • drug effects • drug
             effects* • pharmacology*},
   Abstract = {Guide cannulae for push-pull perfusion were bilaterally
             implanted stereotaxically within the anterior hypothalamic,
             preoptic area (AH/POA) and posterior hypothalamus (PH) of
             the cat. Catecholamine-reactive sites were identified within
             AH/POA in which a microinjection of norepinephrine (NE) (5.0
             micrograms) evoked a characteristic, transient hypothermia.
             Similarly the cation-reactive region within the PH was
             identified in which excess Ca2+ (25 mM) also evoked a
             hypothermic response. When verapamil was perfused at a rate
             of 25.0 microliters/min in a concentration of 0.4 or 2.0
             micrograms/microliter within AH/POA at a NE-sensitive site,
             a concentration-dependent decline in the core temperature of
             the cat occurred. Conversely, verapamil perfused in the same
             manner with a Ca2+-reactive site caused an intense rise in
             the cat's body temperature which also was concentration
             dependent. These results show that the localized blockade of
             slow Ca2+ channels exerts direct, differential physiological
             effects within central nervous system tissue. In this case,
             verapamil mimics noradrenergic effects within the AH/POA;
             however, the hyperthermic response following Ca2+ channel
             blockade within tissue of the PH resembled that produced by
             ethyleneglycoltetraacetic acid or Na ions.},
   Language = {eng},
   Key = {fds275730}
}

@article{fds275731,
   Author = {Myers, RD and Rezvani, AH and Gurley-Orkin, LA},
   Title = {New double-lumen polyethylene cannula for push-pull
             perfusion of brain tissue in vivo.},
   Journal = {Journal of Neuroscience Methods},
   Volume = {12},
   Number = {3},
   Pages = {205-218},
   Year = {1985},
   Month = {January},
   ISSN = {0165-0270},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/2858607},
   Keywords = {Animals • Brain • Caudate Nucleus • Dopamine
             • Hypothalamus • Macaca mulatta •
             Neurotransmitter Agents • Norepinephrine •
             Perfusion • Rats • instrumentation* •
             physiology • physiology*},
   Abstract = {A new concept in the design of a push-pull cannula device
             for localized perfusion of brain tissue in the conscious
             and/or unrestrained animal is described. A catheter,
             consisting of a single strand of polyethylene tubing,
             contains an internal dividing septum which runs
             longitudinally throughout its length. The orifice of each
             lumen is of equal diameter and provides an integrated system
             for simultaneous delivery and withdrawal of a perfusate from
             the perfusion locus. The principal features of the new
             cannula system are: its simplicity of fabrication due to its
             all-plastic construction; multiple tip configurations
             adapted for a specific anatomical requirement including
             V-shaped, slanted, horizontal and side-by-side opening;
             direct visualization of the perfusate monitor bubble through
             the wall of the transparent catheter; since there are no
             joints, lack of leakage of perfusate and occlusion of pull
             channel; ease of sterilization by liquid or gas methods; and
             infrequency of damage because of catheter flexibility. Using
             radiolabeled dopamine and norepinephrine, prototype
             experiments carried out with 3 flow rates and 3 tip
             configurations revealed differences in substrate exchange
             which depend upon a given experimental parameter. The
             practical advantages are discussed of the new perfusion
             system in comparison with dialysis needles as well as with
             more commonly used concentric, metallic push-pull cannulae.
             Finally, technical applications are presented of the methods
             for the rat and other animals in which either the
             pharmacological delivery of a drug over a specified
             interval, or recovery of a neurotransmitter released into
             the cerebral parenchyma is a principal experimental
             objective.},
   Language = {eng},
   Key = {fds275731}
}

@article{fds275728,
   Author = {Rezvani, AH and Heath, JE},
   Title = {Reduced thermal sensitivity in the rabbit by beta-endorphin
             injection into the preoptic/anterior hypothalamus.},
   Journal = {Brain Research},
   Volume = {292},
   Number = {2},
   Pages = {297-302},
   Year = {1984},
   Month = {February},
   ISSN = {0006-8993},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/6318914},
   Keywords = {Animals • Body Temperature Regulation • Brain
             Mapping • Endorphins • Hypothalamus, Anterior
             • Male • Preoptic Area • Rabbits • Skin
             • Thermoreceptors • Vasomotor System •
             beta-Endorphin • blood supply • drug effects
             • drug effects* • innervation •
             pharmacology*},
   Abstract = {Male New Zealand White rabbits, Oryctolagus cuniculus, were
             stereotaxically implanted with a guide tube above the
             preoptic/anterior hypothalamus (PO/AH) for the injection of
             beta-endorphin (beta-E) or saline at ambient temperatures of
             20 and 25 degrees C. Ear skin and PO/AH temperatures were
             recorded in loosely restrained control and beta-E-pretreated
             rabbits while radiant heat was applied to the dorsal skin.
             Without beta-E administration the ear skin temperature
             (Tear) underwent a rapid increase during back heating.
             Following beta-E administration there was a marked
             vasoconstriction along with a large reduction in
             responsiveness of ear skin temperature to radiant heat. The
             time to respond to radiant heat for beta-E-pretreated
             rabbits was significantly longer than that for control
             rabbits. In control animals, the increase in Tear in
             response to radiant heat exposure depended upon the initial
             ear temperatures. However, in beta-E-pretreated rabbits
             vasodilatation response to radiant heat exposure was nearly
             the same regardless of the initial Tear. These data suggest
             that there is a significant reduction in passage of
             temperature information from cutaneous thermal receptors to
             the PO/AH in beta-E-pretreated animals and that
             beta-E-induced reduction in sensitivity of the vasomotor
             system to radiant heat may account for the effectiveness of
             this opioid peptide to promote hyperthermia in the
             rabbit.},
   Language = {eng},
   Key = {fds275728}
}

@article{fds275729,
   Author = {Gordon, CJ and Rezvani, AH and Heath, JE},
   Title = {Role of beta-endorphin in the control of body temperature in
             the rabbit.},
   Journal = {Neuroscience and Biobehavioral Reviews},
   Volume = {8},
   Number = {1},
   Pages = {73-82},
   Year = {1984},
   ISSN = {0149-7634},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/6328389},
   Keywords = {Animals • Body Temperature Regulation • Endorphins
             • Energy Metabolism • Hypothalamus, Anterior
             • Male • Motor Activity • Neurons •
             Preoptic Area • Rabbits • Skin Temperature •
             Vascular Resistance • Vasomotor System •
             beta-Endorphin • drug effects • drug effects*
             • pharmacology*},
   Abstract = {There is evidence of release of the opioid peptide
             beta-endorphin (beta-E) in the hypothalamus during
             development of fever and stress-induced hyperthermia. In the
             unanesthetized rabbit, microinjection of beta-E in the
             preoptic/anterior hypothalamus (POAH) results in peripheral
             vasoconstriction, inhibition of evaporative heat loss, and a
             prolonged elevation of body temperature. These reactions are
             magnified with increases in ambient temperature. Injections
             of beta-E nearly abolish vasodilation to back heating and
             also postural enhancement of heat dissipation ( sprawling ,
             limb extension) in a hot environment. beta-E has also been
             found to reduce the thermal sensitivity of single POAH
             neurons to ambient heating. However, POAH beta-E injections
             do not alter metabolic rate at ambient temperatures from 2
             to 27 degrees C, and to this extent beta-E-induced
             hyperthermia is distinct from fever. It is suggested that
             beta-E reduces sensitivity of POAH neurons to high ambient
             temperature and that this reduction leads to increased
             peripheral vasoconstriction, inhibition of evaporative heat
             loss, and modification of behavioral thermoregulation
             resulting in a regulated-type elevation in body temperature.
             A general neural model is proposed to explain the
             thermoregulatory effects of beta-E in the
             rabbit.},
   Language = {eng},
   Key = {fds275729}
}

@article{fds275725,
   Author = {Rezvani, AH and Gordon, CJ and Heath, JE},
   Title = {Action of preoptic injections of beta-endorphin on
             temperature regulation in rabbits.},
   Journal = {The American Journal of Physiology},
   Volume = {243},
   Number = {1},
   Pages = {R104-R111},
   Year = {1982},
   Month = {July},
   ISSN = {0002-9513},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/6283919},
   Keywords = {Animals • Body Temperature • Body Temperature
             Regulation • Ear • Endorphins • Hypothalamus
             • Kinetics • Male • Naloxone • Preoptic
             Area • Rabbits • Vasoconstriction •
             beta-Endorphin • drug effects • drug effects*
             • pharmacology • pharmacology* •
             physiology*},
   Abstract = {Male New Zealand White rabbits, Oryctolagus cuniculus, were
             stereotaxically implanted with a guide tube above the
             preoptic/anterior hypothalamus area (PO/AH) for the
             injection of the opioid peptide, beta-endorphin (beta-E),
             naloxone, sodium salicylate, or physiological saline. PO/AH
             and ear temperature, oxygen consumption, and evaporative
             heat loss (EHL) were recorded in free-moving rabbits before
             and after injection of saline followed with beta-E,
             naloxone, or sodium salicylate at ambient temperatures (Ta)
             of 2-31 degrees C. A 5-micrograms injection of beta-E
             promoted a rapid reduction in ear temperature followed by a
             prolonged rise in PO/AH (body) temperature. Preinjection
             with an isovolumetric amount of the opiate antagonist,
             naloxone, inhibited the thermoregulatory effects of beta-E.
             The beta-E-induced rise in body temperature was directly
             correlated with Ta. beta-E had no effect on oxygen
             consumption at Ta's of 5 and 27 degrees C. When measured 30
             min after injection, beta-E demonstrated a significant
             inhibition of EHL at Ta's of 27 and 31 but not 5 degrees C.
             The beta-E-induced rise in body temperature was not
             antagonized with preinjections of sodium salicylate in the
             PO/AH. These data indicate that beta-E promotes a regulated
             increase in body temperature. The mechanism of activation
             appears to be distinct from that of an infectious
             fever.},
   Language = {eng},
   Doi = {10.1152/ajpregu.1982.243.1.r104},
   Key = {fds275725}
}

@article{fds275726,
   Author = {Rezvani, AH and Heath, JE},
   Title = {Effect of direct preoptic injections of β-endorphin on
             metabolism, evaporative heat loss, and body temperature in
             the rabbit},
   Journal = {Federation Proceedings},
   Volume = {41},
   Number = {4},
   Pages = {4137-},
   Year = {1982},
   Key = {fds275726}
}

@article{fds275727,
   Author = {Rezvani, AH and Gordon, CJ and Heath, JE},
   Title = {Action of preoptic injections of β-endorphin on temperature
             regulation in rabbits},
   Journal = {American Journal of Physiology - Regulatory Integrative and
             Comparative Physiology},
   Volume = {12},
   Number = {1},
   Pages = {R104-R111},
   Year = {1982},
   Abstract = {Male New Zealand White rabbits, Oryctolagus cuniculus, were
             stereotaxically implanted with a guide tube above the
             preoptic/anterior hypothalamus area (PO/AH) for the
             injection of the opioid peptide, β-endorphin (β-E),
             naloxone, sodium salicylate, or physiological saline. PO/AH
             and ear temperature, oxgyen consumption, and evaporative
             heat loss (EHL) were recorded in free-moving rabbits before
             and after injection of saline followed with β-E, naloxone,
             or sodium salicylate at ambient temperatures (T(a)) of
             2-31° C. A 5-μg injection of β-E promoted a rapid
             reduction in ear temperature followed by a prolonged rise in
             PO/AH (body) temperature. Preinjection with an isovolumetric
             amount of the opiate antagonist, naloxone, inhibited the
             thermoregulatory effects of β-E. The β-E-induced rise in
             body temperature was directly correlated with T(a). β-E had
             no effect on oxygen consumption at T(a)'s of 5 and 27° C.
             When measured 30 min after injection, β-E demonstrated a
             significant inhibition of EHL at T(a)'s of 27 and 31 but not
             5°C. The β-E-induced rise in body temperature was not
             antagonized with preinjections of sodium salicylate in the
             PO/AH. These data indicate that β-E promotes a regulated
             increase in body temperature. The mechanism of activation
             appears to be distinct from that of an infectious
             fever.},
   Key = {fds275727}
}

@article{fds275724,
   Author = {Gordon, CJ and Rezvani, AH and Fruin, ME and Trautwein, S and Heath,
             JE},
   Title = {Rapid brain cooling in the free-running hamster Mesocricetus
             auratus.},
   Journal = {Journal of Applied Physiology: Respiratory, Environmental
             and Exercise Physiology},
   Volume = {51},
   Number = {5},
   Pages = {1349-1354},
   Year = {1981},
   Month = {November},
   ISSN = {0161-7567},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/7298473},
   Keywords = {Animals • Body Temperature Regulation* • Brain
             • Cricetinae • Male • Mesocricetus •
             Physical Exertion* • physiology*},
   Abstract = {A thermocouple reentrant tube was stereotaxically implanted
             in the rostral brain stem of the golden hamster,
             Mesocricetus auratus. Brain temperature was continuously
             recorded while the hamster was permitted volitional running
             on an activity wheel. There was an immediate decrease in
             brain temperature at the start of running activity, reaching
             a mean of 0.49 degrees C below the prerunning level.
             Spontaneous or forced cessation of running activity was
             associated with a rapid recovery of brain temperature. The
             time course of brain cooling during exercise greatly
             differed from the exponential decay of brain temperature in
             hyperthermic and dead animals. Air flow through the nose may
             contribute to the maintenance of a low brain temperature
             because nasal blockade promotes an increase in brain
             temperature. Below an ambient temperature of 33 degrees C,
             the resting hamster maintains its brain temperature below
             deep-body (abdominal) temperature. Vinyl acetate casts of
             the arterial and venous systems revealed several potential
             sites for heat exchange that might account for brain cooling
             under resting and exercising conditions.},
   Language = {eng},
   Doi = {10.1152/jappl.1981.51.5.1349},
   Key = {fds275724}
}

@article{fds275723,
   Author = {Rezvani, AH and Gordon, CJ and Heath, JE},
   Title = {Action of direct preoptic/anterior hypothalamus injections
             of beta-endorphin on temperature regulation in awake
             rabbits},
   Journal = {Federation Proceedings},
   Volume = {40},
   Number = {3 I},
   Pages = {No.-1178},
   Year = {1981},
   Month = {January},
   Key = {fds275723}
}


%% Chapters in Books   
@misc{fds340176,
   Author = {Levin, ED and Rezvani, AH},
   Title = {Nicotinic involvement in cognitive function of
             rats},
   Pages = {167-178},
   Booktitle = {Nicotinic Receptors in the Nervous System},
   Year = {2001},
   Month = {January},
   ISBN = {084932386X},
   Abstract = {© 2002 by CRC Press LLC. Rat models have been very useful
             in demonstrating the effects of nicotinic agonist and
             antagonist on memory performance. Experimental rat models
             have been critical in providing the behavioral
             characterization of nicotinic effects on memory, as well as
             important data concerning the anatomic loci, nicotinic
             receptor subtypes, and neurotransmitter interactions
             important for nicotinic effects on memory. A variety of
             studies with rats have shown that nicotine and other
             nicotinic agonists can improve memory performance, while
             nicotinic antagonists such as mecamylamine can impair it
             (see references for reviews). This research provides an
             important bridge between studies of the biochemical studies
             of nicotinic receptor function and studies of potential
             clinical application of nicotinic therapies for memory
             impairment.},
   Key = {fds340176}
}


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