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Strychnine interactions with acetylcholine, dopamine and serotonin receptors in Aplysia neurons
Authors:D S Faber  M R Klee
Affiliation:1. Max-Planck-Institut fu¨r Hirnforschung, Neurobiologische Abteilung, Frankfurt/M-Niederrad G.F.R.;2. Neurosensory Laboratory, Department of Physiology, State University of New York at Buffalo, Buffalo, N.Y. U.S.A.
Abstract:The effects of strychnine on synaptic transmission in the abdominal ganglion ofAplysia californica and on the responses of individual neurons to iontophoretic application of acetylcholine, dopamine and serotonin were studied using conventional techniques of intracellular recording. Strychnine inhibited all classical (relatively short-lasting) excitatory and inhibitory postsynaptic potentials as well as the various sodium- and chloride-dependent phoresis responses. Only the potassium-dependent inhbitions of prolonged duration, activated in some cells transsynaptically or by dopamine or acetylcholine application, were not antagonized; sometimes these inhibitions were enhanced. Log-dose-response curves indicated that for each of the 3 drugs the depolarizing responses were more sensitive to strychnine than were the hyperpolarizing responses. Also, a given strychnine concentration generally inhibited the serotonin and dopamine responses to a greater extent than the acetylcholine responses.The antagonism by strychnine of the Na+- and Cl?-dependent phoresis responses — similar to the action of curare on these receptors — is apparently due to selective interactions with some membrane receptors for the applied drugs.Finally, the limitations to the analysis of the dose-response curves generated by the iontophoretic technique are briefly discussed. It is suggested that the strychnine inhibitions of the acetylcholine and dopamine depolarizing responses might be due to a competitive inhibitory action, whereas in respect to the changes in their dose-response curves, the chloride-dependent ACh-H response and the 5-HT-D and H responses of these receptors seem to be blocked by a non-competitive action of the drug.
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