Effects of met-enkephalin on slow synaptic inhibition in frog sympathetic ganglion

Abstract

The influence of met-enkephalin on slow inhibitory postsynaptic potentials (IPSP) in the frog sympathetic ganglion was studied with the help of a sucrose gap technique. Application of 1 μM met-enkephalin caused a hyperpolarization of the ganglionic neurones, probably via a postsynaptic mechanism. In addition, met-enkephalin depressed the amplitude of the slow IPSP by 40%. Both effects were completely antagonized by 1 μM naloxone. -ala-met-enkephalinamide (1 μM) and morphine (5 μM) also produced a hyperpolarization together with a depression of the slow IPSP. By varying the external potassium concentration it was shown that the depression of the slow IPSP was not due to the hyperpolarization of the ganglionic neurones by met-enkephalin. Further experimentation revealed that the sensitivity of the ganglion to exogenous dopamine, the putative transmitter for the slow IPSP, was only slightly suppressed by met-enkephalin. It is concluded that the depression of the slow IPSP by met-enkephalin is presynaptic in origin and may be the result of a decrease in the amount of transmitter released from the nerve terminals. The possibility that the reduction in transmitter release is brought about by a hyperpolarization of the nerve terminals is discussed. A hyperpolarization of the preganglionic nerve terminals was actually observed after application of 5 μM morphine.