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ISBRA 2004 Abstracts
The Scripps Research Institute, La Jolla
ACUTE AND CHRONIC ETHANOL ALTER GABA AND GLUTAMATE NEUROTRANSMISSION
Roberto M., Schweitzer P., Madamba S.G., Stouffer D.G., Parsons L.H. and Siggins G.R. (2004) . Alcohol Clin. Exp. Res. Suppl. Vol. ISBRA 28: 13.17.
Department of Neuropharmacology, The Scripps Research Institute, La Jolla, CA
The central nucleus of amygdala (CeA) is a brain region involved in ethanol reward and dependence. Here we used the in vitro CeA slice preparation and in vivo brain microdialysis to study the interaction of acute ethanol with the GABAergic and glutamatergic systems, in rats subjected to chronic ethanol treatment (CET; 2-3 weeks) via ethanol inhalation. In CeA neurons of CET rats, acute superfusion of ethanol (11-66 mM) enhanced GABAA-IPSP/Cs, with recovery on washout. The ethanol effect on IPSP/Cs was quantitatively similar to that in neurons from naive rats, suggesting a lack of tolerance. In CET rats, however, the overall amplitude of evoked IPSP/Cs was larger, spontaneous IPSP/C activity was increased, and baseline paired-pulse facilitation (PPF) of IPSP/Cs was decreased compared to naive rats, suggesting that evoked GABA release was increased after CET. We also found that in CET neurons the inhibition of NMDA-EPSP/Cs by acute ethanol was greater and associated with a reduction of PPF, suggesting neuroadaptative changes in ethanol-induced glutamate release after CET. In vivo administration of ethanol (0.1, 0.3, 1.0 M) via a microdialysis probe produced a dose-dependent increase of GABA release in CeA dialysates of both CET and naive rats, but increased glutamate release only in CET rats. Moreover, in CET rats baseline GABA and glutamate dialysate contents were higher (4 fold and 2 fold, respectively) compared to naive rats. These electrophysiological and microdialysis findings suggest that the development of ethanol dependence elicits neuroadaptations at GABAergic and glutamatergic CeA synapses, and may underly behavioral signs of ethanol dependence. Supported by grants from NIH (AA013517, AA06420, DA03665, AA12294).
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