High-frequency stimulation induces ethanol-sensitive long-term potentiation at glutamatergic synapses in the dorsolateral bed nucleus of the stria terminalis.

Weitlauf C, Egli RE, Grueter BA, Winder DG
J Neurosci. 2004 24 (25): 5741-7

PMID: 15215296 · PMCID: PMC6729219 · DOI:10.1523/JNEUROSCI.1181-04.2004

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.

MeSH Terms (15)

Animals Calcium Channels, L-Type Electric Stimulation Electrophysiology Ethanol Glutamic Acid In Vitro Techniques Long-Term Potentiation Male Mice Mice, Inbred C57BL Receptors, GABA-A Receptors, N-Methyl-D-Aspartate Septal Nuclei Synapses

Connections (1)

This publication is referenced by other Labnodes entities: