Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1997-7-22
pubmed:abstractText
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 suppressive 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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0145-6008
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
368-74
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Ethanol inhibits single-unit responses in the nucleus accumbens evoked by stimulation of the basolateral nucleus of the amygdala.
pubmed:affiliation
Alcohol Research Center, Scripps Research Institute, La Jolla, California 92037, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.