Publications [#333703] of Michael C. Reed

Papers Published

1. Suppiramaniam, V; Bloemer, J; Reed, M; Bhattacharya, S, Neurotransmitter Receptors, in Comprehensive Toxicology: Third Edition, vol. 6-15 (January, 2018), pp. 174-201, Elsevier, ISBN 9780081006016 [doi]
   (last updated on 2024/04/18)

   Abstract:
   Neurotransmitter receptors play a vital role in the normal functioning of the nervous system. Controlled modulation of neurotransmitter receptors is critical for proper signaling between nerve cells and effector organs. Factors that disrupt normal neurotransmitter signaling can alter the homeostasis of the cells or tissues, leading to adverse effects. The release of neurotransmitters at the presynaptic neuron and the subsequent activation of postsynaptic receptors lead to stimulation or inhibition of neuronal transmission. The excitatory neurotransmission involves depolarization of the postsynaptic neuron or cell due to a decrease in the polarity of the cells by the influx of cations such as sodium ions. The excitatory neurotransmission is mainly carried out by glutamate receptors in the mammalian nervous system. The inhibitory neurotransmission is due to hyperpolarization of the cells by either influx of anions such as chloride ions or efflux of cations such as potassium ions. The GABA and glycine receptors serve as major inhibitory neurotransmitter receptors. Toxins and toxicants can interfere with neuronal transmission by directly binding receptors and modulating their function or by altering transmitter synthesis, release, and reuptake mechanisms. Therefore, neurotoxins can impair neuronal transmission at the synapse by either presynaptic modulation or postsynaptic modifications. Due to the intricate network of the nervous system, impairment of the receptor functions in the synapse can lead to regional network dysfunction, eventually resulting in adverse cellular effects and behavioral deficits. Therefore, a thorough knowledge of neurotransmitter receptor modulation by toxins and toxicants is essential for future development of therapies against adverse effects of these neurotoxic substances.