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Ethanol augments GABAergic transmission in the central amygdala via CRF1 receptors

Academic Article
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Overview

authors

  • Nie, Z. G.
  • Schweitzer, Paul
  • Roberts, Amanda
  • Madamba, S. G.
  • Moore, S. D.
  • Siggins, George

publication date

  • March 2004

journal

  • Science  Journal

abstract

  • The central amygdala (CeA) plays a role in the relationship among stress, corticotropin-releasing factor (CRF), and alcohol abuse. In whole-cell recordings, both CRF and ethanol enhanced gamma-aminobutyric acid-mediated (GABAergic) neurotransmission in CeA neurons from wild-type and CRF2 receptor knockout mice, but not CRF1 receptor knockout mice. CRF1 (but not CRF2) receptor antagonists blocked both CRF and ethanol effects in wild-type mice. These data indicate that CRF1 receptors mediate ethanol enhancement of GABAergic synaptic transmission in the CeA, and they suggest a cellular mechanism underlying involvement of CRF in ethanol's behavioral and motivational effects.

subject areas

  • Alcohol Drinking
  • Amygdala
  • Animals
  • Corticotropin-Releasing Hormone
  • Dose-Response Relationship, Drug
  • Ethanol
  • Evoked Potentials
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Neurons
  • Patch-Clamp Techniques
  • Receptors, Corticotropin-Releasing Hormone
  • Receptors, GABA-A
  • Stress, Psychological
  • Synaptic Transmission
  • gamma-Aminobutyric Acid
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Identity

International Standard Serial Number (ISSN)

  • 0036-8075

Digital Object Identifier (DOI)

  • 10.1126/science.1092550

PubMed ID

  • 15001778
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Additional Document Info

start page

  • 1512

end page

  • 1514

volume

  • 303

issue

  • 5663

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