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.
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