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Ethanol augments GABAergic transmission in the central amygdala via CRF1 receptors.

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Affiliations

  • 1. Department of Neuropharmacology and Alcohol Research Center, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
      Authors
    • Nie Z 1
    (1 author)

Science, 01 Mar 2004, 303(5663):1512-1514
https://doi.org/10.1126/science.1092550 PMID: 15001778 

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.

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Read article at publisher's site: https://doi.org/10.1126/science.1092550

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Funding 

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NIAAA NIH HHS (2)

NIDA NIH HHS (2)