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Ethanol Augments GABAergic Transmission in the Central Amygdala via CRF1 Receptors

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Science  05 Mar 2004:
Vol. 303, Issue 5663, pp. 1512-1514
DOI: 10.1126/science.1092550

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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 γ-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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