Involvement of an interneuron in the generation of the slow inhibitory postsynaptic potential in mammalian sympathetic ganglia.

Abstract

Acetylcholine (AcCho) was applied electrophoretically to cells of isolated rabbit superior cervical ganglia, and the response was recorded by means of intracellular recording techniques. In the presence of d-tubocurarine (5 .mu.M), AcCho applied by tetanic current pulses elicited 3 distinct membrane potential changes: a slow depolarization, a slow hyperpolarization, and a biphasic response consisting of an initial hyperpolarization followed by a depolarization. Atropine (1 .mu.M) abolished all the membrane potential changes elicited by AcCho. On the contrary, superfusion with a low-Ca/high-Mg solution, tetrodotoxin (0.1 .mu.M), or haloperidol (0.1 .mu.M) selectively and reversibly blocked AcCho-induced hyperpolarization without appreciably affecting the depolarization. The membrane resistance remained relatively constant during the course of hyperpolarization. Application of steady depolarizing and hyperpolarizing currents decreased and increased, respectively, the amplitude of hyperpolarization. The hyperpolarization elicited by AcCho is electrophysiologically and pharmacologically similar to the slow inhibitory postsynaptic potential induced by nerve stimulation. Slow inhibitory postsynaptic potential elicited by presynanptic stimulation is a disynaptic phenomenon involving the release of a second transmitter, possibly dopamine, from an interneuron.