Opiate and alpha 2-adrenoceptor responses of rat amygdaloid neurons: co-localization and interactions during withdrawal.

Interactions between neuronal responses mediated by opiate receptors and by alpha 2-adrenoceptors were characterized in the amygdala. Extracellular single-unit recordings and microiontophoresis were performed using five-barrel microelectrodes in chloral hydrate-anesthetized rats. A subpopulation of amygdaloid cells displayed inhibitory responses to morphine or D-Ala,D-Leu-enkephalin; antagonist studies suggested that both mu- and delta-opiate receptor subtypes were present. The same neurons displayed inhibitory responses to norepinephrine or clonidine mediated by alpha 2-adrenoceptors. Responses mediated by opiate receptors and by alpha 2-adrenoceptors were highly co-localized to the same subpopulation of amygdaloid neurons. Such cells responded to microiontophoresis of either morphine or clonidine, whereas other cells in the amygdala generally showed neither response. Responsive cells were characterized by a distinctive, triphasic waveform and a high sensitivity to glutamate. These cells were largely restricted to the nucleus centralis and the posterior portion of the nucleus medialis. Cells outside of this group showed suppressant responses to norepinephrine which appeared not to be mediated by alpha 2-adrenoceptors. After chronic morphine treatment, application of opioid antagonists elicited a withdrawal response, consisting of an increase in firing rate. Clonidine reversed the withdrawal response of these cells. The amygdala may be one of the regions of the nervous system in which clonidine acts to reduce symptoms of opiate withdrawal.