Journal
JOURNAL OF NEUROSCIENCE
Volume 24, Issue 25, Pages 5741-5747Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1181-04.2004
Keywords
alcohol; alcoholism; synaptic plasticity; stress; anxiety; addiction
Categories
Funding
- NIAAA NIH HHS [R01 AA019455] Funding Source: Medline
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available