Muscarinic receptor regulation of synaptic transmission in airway
parasympathetic ganglia.
Myers, Allen C., and Bradley J. Undem.
Division of Clinical Immunology, The Johns Hopkins Asthma and
Allergy Center, 5501 Hopkins Bayview Circle 3A.62, Baltimore, MD
21224
APStracts 2:0213L, 1995.
Muscarinic receptor regulation of synaptic transmission in guinea pig
bronchial parasympathetic ganglia was evaluated using intracellular
recording of the intrinsic ganglion neurons. Methacholine (1[mu]M)
decreased the amplitude of vagus nerve-stimulated fast excitatory
postsynaptic potentials (fEPSPs) by 33% and 46% (at 0.8 and 8.0 Hz,
respectively), but had no effect on the amplitude of the
depolarizations evoked by a bath applied nicotinic receptor agonist.
Methoctramine (1[mu]M) inhibited methacholine's effect on fEPSPs, but
alone did not influence the magnitude of the fEPSPs evoked by vagus
nerve stimulation. Methacholine (10[mu]M) depolarized a sub
-population of neurons (about 4 mV), which was blocked by pirenzepine
(0.1[mu]M), in other neurons either no effect or a small (1-5mV)
hyperpolarization was noted. Cholinergic contractions of bronchial
smooth muscle elicited by electrical field stimulation were
potentiated by methoctramine to the same extent as those evoked by
vagus nerve (preganglionic) stimulation. The data indicate that M2
receptor activation can lead to inhibition of presynaptic
acetylcholine release and consequently a significant inhibition of
synaptic transmission in bronchial parasympathetic ganglia. The
physiological role of this neuromodulatory effect appears limited,
however, when studied in the in vitro setting.
Received 17 July 1995; accepted in final form 8 November 1995.
APS Manuscript Number L221-5.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 December 95