期刊
JOURNAL OF NEUROSCIENCE
卷 24, 期 25, 页码 5741-5747出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1181-04.2004
关键词
alcohol; alcoholism; synaptic plasticity; stress; anxiety; addiction
资金
- NIAAA NIH HHS [R01 AA019455] Funding Source: Medline
Anatomical and functional data support a critical role for the bed nucleus of the stria terminalis (BNST) in the interaction between stress and alcohol/substance abuse. We report here that neurons of the dorsal anterolateral BNST respond to glutamatergic synaptic input in a synchronized way, such that an interpretable extracellular synaptic field potential can be readily measured. High-frequency stimulation of these glutamatergic inputs evoked NMDA receptor (NMDAR)-dependent long-term potentiation (LTP). We found that an early portion of this LTP is reduced by acute exposure to ethanol in a GABA(A) receptor-dependent manner. This effect of ethanol is accompanied by a significant and reversible dose-dependent attenuation of isolated NMDAR signaling and is mimicked by incomplete NMDAR blockade.
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