Publications [#268481] of Dale Purves

Papers Published

1. Purves, D (1976). Functional and structural changes in mammalian sympathetic neurones following colchicine application to post-ganglionic nerves.. The Journal of Physiology, 259(1), 159-175. [doi]
   (last updated on 2023/06/01)

   Abstract:
   1. The effects of post-ganglionic colchicine application on neurones of the guinea-pig superior cervical ganglion were studied with intracellular recording and electron microscopy. 2. Local colchicine application for 30 min to one of the major post-ganglionic nerves caused several electrophysiological changes after 4-7 days in many neurones whose axons run in this nerve. These changes include: (a) a reduction in the amplitude of synaptic potentials elicited by supramaximal preganglionic stimulation; (b) a decrease in the number of preganglionic fibres innervating individual neurones; (c) the development of regenerative responses in dendrites; and (d) the failure of antidromic action potentials to fully invade the neuronal soma. These functional changes occurred in the absence of impaired impulse conduction or axon degeneration, and were not observed in nearby neurones whose axons ran in an untreated post-ganglionic nerve. The effects of colchicine are similar to the changes produced by axotomy. 3. Counts of synapses in thin sections from the region of the ganglion where the affected neurones were located showed a reduction, compared to the number of synapses in other regions of the colchicine treated ganglia, or normal control ganglia. This finding indicates that synaptic depression after colchicine treatment, like that after axotomy, is due primarily to a loss of synaptic contacts from the dendrites of affected nerve cells. Unusual profiles containing numerous vesicular and tubular organelles frequently seen after interruption of the axons were also observed in thin sections after colchicine treatment. 4. The similarity of the electrophysiological and ultrastructural effects of colchicine treatment and axon interruption offers further support for the view that synaptic contacts on sympathetic neurones are normally regulated by an interaction of the neuronal soma with its axonal extension to the periphery.