MUSCARINIC RECEPTOR REGULATION OF SYNAPTIC TRANSMISSION IN AIRWAY PARASYMPATHETIC GANGLIA

Muscarinic receptor regulation of synaptic transmission in guinea pig bronchial parasympathetic ganglia was evaluated with the use of intrac ellular recording of the intrinsic ganglion neurons. Methacholine (1 m u M) decreased the amplitude of vagus nerve-stimulated fast excitatory postsynaptic potentials (fEPSP) by 33 and 46% (at 0.8 and 8.0 Hz, res pectively) but had no effect on the amplitude of the depolarizations e voked by a bath-applied nicotinic receptor agonist. Methoctramine (1 m u M) inhibited methacholine's effect on fEPSP but alone did not influe nce the magnitude of the fEPSP evoked by vagus nerve stimulation. Meth acholine (10 mu M) depolarized a subpopulation of neurons (similar to 4 mV), which was blocked by pirenzepine (0.1 mu M). In other neurons, either no effect or a small (1-5 mV) hyperpolarization was noted. Chol inergic contractions of bronchial smooth muscle elicited by electrical field stimulation were potentiated by methoctramine to the same exten t as those evoked by vagus nerve (preganglionic) stimulation. The data indicate that M(2) receptor activation can lead to inhibition of pres ynaptic acetylcholine release and consequently a significant inhibitio n of synaptic transmission in bronchial parasympathetic ganglia. The p hysiological role of this neuromodulatory effect appears limited, howe ver, when studied in the in vitro setting.