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

Zhiguo Nie, Paul Schweitzer, Amanda J Roberts, Samuel G Madamba, Scott D Moore, George Robert Siggins

文献索引：Science 303 , 1512-1514, (2004)

全文：HTML全文

摘要

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.