Ethanol augments GABAergic transmission in the central amygdala via CRF1 receptors

  • Science. 2004 Mar 5;303(5663):1512-4. doi: 10.1126/science.1092550.
Zhiguo Nie  1 ,  Paul Schweitzer ,  Amanda J Roberts ,  Samuel G Madamba ,  Scott D Moore ,  George Robert Siggins
Affiliations
  • 1. Department of Neuropharmacology and Alcohol Research Center, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
PMID: 15001778 DOI: 10.1126/science.1092550
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.