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PRESYNAPTIC MUSCARINIC RECEPTORS INHIBITING ACTIVE ACETYLCHOLINE RELEASE IN THE BULLFROG SYMPATHETIC GANGLION
Author(s) -
KOKETSU K.,
YAMADA M.
Publication year - 1982
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1982.tb09271.x
Subject(s) - bethanechol , sympathetic ganglion , bullfrog , muscarinic acetylcholine receptor , acetylcholine , chemistry , endocrinology , excitatory postsynaptic potential , postsynaptic potential , muscarine , medicine , atropine , depolarization , phentolamine , biology , inhibitory postsynaptic potential , receptor , propranolol
1 The effects of bethanechol and atropine on the release of acetylcholine (ACh) from bullfrog sympathetic preganglionic nerve terminals were examined electrophysiologically. 2 Bethanechol (1 m m ) caused no depolarization of sympathetic preganglionic nerve terminals, whereas carbachol or ACh in the same concentration induced marked depolarizations of these terminals. 3 Bethanechol (10 μ m ) depressed the amplitude of fast excitatory postsynaptic potentials (e.p.s.ps) recorded in low Ca 2+ ‐high Mg 2+ solution, without depolarizing ganglion cells. The quantal content measured from these fast e.p.s.ps by the variance method showed a significant reduction. 4 Amplitudes of both miniature e.p.s.ps and ACh‐potentials induced by iontophoresis of ACh were not affected by addition of bethanechol (10 μ m ). 5 The depressant effect of bethanechol (10 μ m ) on fast e.p.s.ps disappeared in the presence of atropine (3 μ m ). 6 Atropine (3 μ m ) increased the quantal content measured from fast e.p.s.ps recorded in low Ca 2+ ‐high Mg 2+ solution. 7 The depressant effect of bethanechol (10 μ m ) on fast e.p.s.ps was unaffected by α‐adrenoceptor blocking agents (phenoxybenzamine (10 μ m ) or phentolamine (10 μ m )). 8 These results suggest that presynaptic nerve terminals in bullfrog sympathetic ganglia possess a muscarinic receptor which inhibits active release of ACh.