Sites and mechanisms of actions of enkephalin in the feline parasympathetic ganglion.

Intracellular recordings were made in vitro from neurones of the cat parasympathetic ciliary ganglion with a current- or voltage-clamp technique. (Met5)enkephalin and (leu5)enkephalin (10 nM to 10 microM) were applied by superfusion. Both caused a membrane hyperpolarization which persisted in a calcium-free/high-magnesium solution, and both reduced the amplitude of excitatory post-synaptic potentials (e.p.s.p.s). These actions of enkephalin were antagonized by naloxone. The enkephalin-induced hyperpolarization was associated with an increase in membrane conductance, reversed in polarity at -90 mV and was not altered by changing external sodium and chloride concentrations. This indicates that the enkephalin hyperpolarization is due mainly to activation of potassium conductance. Enkephalin decreased the mean quantal content of e.p.s.p.s recorded in low-calcium/high-magnesium solution, without changing quantal size. Furthermore, the increase in the frequency of miniature e.p.s.p.s after tetanic preganglionic stimulations was inhibited by enkephalin. Acetylcholine potentials were not altered by enkephalin. These findings suggest that enkephalin reduces transmitter release. The experiments suggest that enkephalin may inhibit ganglionic transmission by both pre- and post-synaptic actions in a mammalian parasympathetic ganglion.