Hyperpolarizing action of enkephalin on neurons in the dorsal motor nucleus of the vagus, in vitro

Abstract

Intracellular recordings were made from neurons of the dorsomotor vagal nucleus (DMV) in slices of rat medulla oblongata. [D-Ala 2, D-Leu 5]-enkephalin (DADLE), applied by perfusion (0.01–3 μM) or droplets, dose-dependently hyperpolarized 85% of the DMV neurons tested. The hyperpolarization, associated with a decrease in membrane resistance, persisted after elimination of synaptic activity by perfusion with Ca 2+-free/high-Mg 2+ solution or with 1 μM TTX solution. The opioid antagonist, naloxone, reversibly inhibited DADLE-induced hyperpolarization. The hyperpolarization depended on extracellular K + concentration and reversed at about −90 mV. DADLE also decreased Ca 2+-dependent spike duration and after-hyperpolarization (AHP). DAGO (a selective μ-receptor agonist), but not DPLPE (a selective δ-receptor agonist), mimicked DADLE's effects on membrane potential, Ca 2+-dependent spike duration, and AHP. It is concluded that DADLE, through postsynaptic μ-type opioid receptors, hyperpolarized DMV neurons by increasing K + conductance, which may have an inhibitory effect on DMV output. DADLE-induced decrease of spike duration and AHP was also mediated by μ-receptors and could have additional effects on functions of the DMV neuron by virtue of reduction in Ca 2+ entry.