Direct excitatory opiate effects mediated by non-synaptic actions on rat medial vestibular neurons

Abstract

Opiates increase firing of rat medial vestibular nucleus neurons. We have attemped to dermined the mechanism of these excitatory opiate actions by extracellular recording of neronal activity with ionophoretic application of opiate agonists and bath application of antagonists. The spontaneous activity of approximately 30% of medial vestibular neurons, scattered throughout nucleus, was increased by ionophoretic application of either morphine or [D-Ala 2]leucine enkephalin, implicating the presence of both mu and delta opiate receptors. The responses to both were blocked by the opiate receptors antagonist, naloxine. In only a few neuron opiates decrease firing. Most previous reports of direct opiate excitation have proven to be due to disinhibition. This is not the case here, as indicated by three observations: 1) the excitatory opiate response was sustained when γ-aminobutyric acid (GABA) receptors were blocked by Bicuculline; 2) perfusion of a solution containing 0.1 nM Ca 2+ and mM Mg 2+ blocks synaptic transmission, but does noe block the excitatory responses to both opiates and 3) the opiate-induced depolarization and action potential generation was evident in neurons whose spontaneous firing was almost totally depressed by adenosine. These results indicate that the excitation is neither due to disinhibition nor to a presynaptic opiate action. We conclude that medial vestibular neuron have postsynaptic opiate receptors that mediate direct neuronal excitation.