Muscarinic cholinergic regulation of cyclic guanosine 3,5-monophosphate in autonomic ganglia: possible role in synaptic transmission.

The effects of acetylcholine, and of agents which selectively mimic or block its nicotinic and muscarinic actions, have been studied on the levels of guanosine 3,5-monophosphate (cyclic GMP) and adenosine 3,5-monophosphate (cyclic AMP) in slices of bovine superior cervical ganglion. Low doses of either acetylcholine or the muscarinic agonist, bethanechol, caused a substantial increase in the level of cyclic GMP, and slightly increased the level of cyclic AMP; the acetylcholine- and the bethanechol-induced increases in cyclic GMP were blocked by atropine, the muscarinic antagonist, but not by hexamethonium, the nicotinic antagonist. The nicotinic agonist N,N-dimethylphenylpiperazinium did not alter the level of either of the cyclic nucleotides. Dopamine increased the level of cyclic AMP and acetylcholine partially prevented this dopamine-induced increase in cyclic AMP. The data are consistent with a model for the ganglion in which muscarinic cholinergic synaptic transmission is mediated by an increase in the level of cyclic GMP in the postganglionic neurons and dopaminergic transmission by an increase in the level of cyclic AMP in these neurons.