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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2004-3-30
pubmed:abstractText
Although ethanol has been reported to inhibit the induction of long-term potentiation in hippocampal CA1 and dentate gyrus synapses of rats, very little is known about the effect of ethanol on synaptic plasticity in other brain regions. Therefore, in the present study, we investigated the effect of ethanol on long-term potentiation in synaptic pathway from the basolateral amygdala to the dentate gyrus by using anesthetized rats in vivo. I.v. (20-40% x 2 ml/kg) or i.c.v. (30-40% x 5 microl) administration of ethanol did not affect the basal amplitude of dentate gyrus field potential evoked by basolateral amygdala stimulation, but significantly inhibited the induction of long-term potentiation following application of tetanic stimulation. Since long-term potentiation in this pathway was independent of N-methyl-d-aspartate receptors, the inhibitory effect of ethanol is unlikely to be caused by suppression of N-methyl-d-aspartate receptor function. Alternatively, long-term potentiation in this pathway was significantly suppressed by the benzodiazepine agonist diazepam (2 mg/kg, i.p.), and the inhibitory effect of ethanol was abolished by the GABAA receptor channel blocker picrotoxin (1 mg/kg, i.p.). The present study demonstrates that ethanol inhibits the induction of long-term potentiation in the basolateral amygdala-dentate gyrus pathway by enhancing GABAA receptor-mediated neurotransmission.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
125
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
113-7
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
GABAA receptor-mediated inhibition by ethanol of long-term potentiation in the basolateral amygdala-dentate gyrus pathway in vivo.
pubmed:affiliation
Department of Pharmacology, School of Pharmacy, Hoshi University, 2-4-41 Ebara, Shinagawa-ku, Tokyo 142-8501, Japan. abe@hoshi.ac.jp
pubmed:publicationType
Journal Article