Distinct muscarinic mediation of suspected dopaminergic activity in sympathetic ganglions.

The competitive neuromuscular blocking agents, gallamine and pancuronium, enhanced the nictitating membrane contraction, in the cat, resulting from muscarine ganglionic transmission. Inhibition of ganglionic muscarinic hyperpolarization, in response to short tetanic bouts of preganglionic cervical sympathetic stimulation, was an associated event and is considered by us to be causally related. The neuroleptic drug, haloperidol, enhanced ganglionic hyperpolarization under similar stimulatory conditions, and reduced the nictitating membrane contraction elicited via ganglionic muscarine pathways, effects opposite to those produced by the skeletal muscle relaxants. Apomorphine reduced both ganglionic hyperpolarization and the ganglionic muscarinic-induced nictitating membrane contractions. The action of gallamine and pancuronium conforms to a speculative cholinergic antagonism at the specific muscarinic receptors, termed Mi, on the ganglionic dopaminergic interneuron. Haloperiodol and apomorphine are anticipated to be exerting distinct antagonistic and agonistic actions, respectively, on prejunctional dopamine receptors of the ganglionic interneuron. Ganglionic slow depolarization mediated through the muscarinic receptors, termed Me, was unaltered by any of the agents studied.