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Ethanol Inhibits Single‐Unit Responses in the Nucleus Accumbens Evoked by Stimulation of the Basolateral Nucleus of the Amygdala
Author(s) -
Criado José R.,
Lee RongSheng,
Berg Greta I.,
Henriksen Steven J.
Publication year - 1997
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1997.tb03775.x
Subject(s) - nucleus accumbens , basolateral amygdala , amygdala , (+) naloxone , stimulation , excitatory postsynaptic potential , chemistry , inhibitory postsynaptic potential , neuroscience , medicine , endocrinology , pharmacology , opioid , receptor , central nervous system , psychology
We studied the actions of intoxicating doses of ethanol on excitatory inputs from the basolateral nucleus of the amygdala, a major afferent system projecting to the nucleus accumbens (NAcc). In view of the hypothesized role of opioid receptors on the effects of ethanol on NAcc physiology, we also explored whether naloxone modulates ethanol‐induced suppression of NAcc excitability in halothane anesthetized and freely moving unanesthetized rats. Intraperitoneal administration of ethanol (1.2–1.4 g/kg) markedly suppressed a subgroup of amygdala‐activated NAcc neurons. The ethanol‐induced reduction in amygdala‐activated NAcc neurons was not reversed by naloxone (5.0 mg/kg, intraperitoneally). Moreover, naloxone had no effect on the supressive effects of ethanol on NAcc spontaneous activity in either halothane‐anesthetized or unanesthetized freely moving preparations. These findings suggest that opiate mechanisms either are not participating or are not solely responsible for the inhibitory effects of acute intoxicating doses of ethanol on NAcc physiology.