AJP - Regulatory, Integrative and Comparative Physiology, Vol 264, Issue 6 1084-R1088, Copyright © 1993 by American Physiological Society
Modulation of release of [3H]acetylcholine in the major pelvic ganglion of the rat
G. T. Somogyi and W. C. de Groat
Department of Pharmacology, University of Pittsburgh, Pennsylvania 15261.
Cholinergic modulation of [3H]acetylcholine release evoked by electrical
stimulation was studied in the rat major pelvic ganglion, which was
prelabeled with [3H]choline. Acetylcholine (ACh) release was independent of
the frequency of stimulation; 0.3 Hz produced the same volley output as 10
Hz. Tetrodotoxin (1 microM) or omission of Ca2+ from the medium abolished
ACh release. The M1 receptor agonist
(4-hydroxy-2-butynyl)-1-trimethylammonium m-chlorocarbanilate chloride
(McN-A 343, 50 microM) increased release (by 136%), whereas the M2
muscarinic agonist oxotremorine (1 microM) decreased ACh release (by 22%).
The muscarinic antagonists, atropine (1 microM) or pirenzepine (M1
selective, 1 microM), did not change ACh release. However, pirenzepine (1
microM) blocked the facilitatory effect of McN-A 343, and atropine (1
microM) blocked the inhibitory effect of oxotremorine. The cholinesterase
inhibitor physostigmine (1-5 microM), the nicotinic agonist
1,1-dimethyl-4-phenylpiperazinium (DMPP, 10 microM), and the nicotinic
antagonist D-tubocurarine (50 microM) did not change ACh release.
4-Aminopyridine, a K+ channel blocker, significantly increased the release
(by 146%). Seven days after decentralization of the major pelvic ganglion,
the evoked release of ACh was abolished. It is concluded that release of
ACh occurs from the preganglionic nerve terminals rather than from the
cholinergic cell bodies and is not modulated by actions of endogenous ACh
on either muscarinic or nicotinic autoreceptors. These data confirm and
extend previous electrophysiological findings indicating that synapses in
the major pelvic ganglion have primarily a relay function.
