Journal of Neuroscience, Vol 5, 3016-3024, Copyright © 1985 by Society for Neuroscience
Opiate and alpha 2-adrenoceptor responses of rat amygdaloid neurons: co- localization and interactions during withdrawal
JE Freedman and GK Aghajanian
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.