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.
![4-(N-ETHYL-N-4-HYDROXYBUTYL)AMINO-2,5,6-TRIMETHYL-7-(2,4,6-TRIMETHYLPHENYL)PYRROLO[2,3-D]PYRIMIDINE HYDROCHLORIDE 结构式](https://image.chemsrc.com/caspic/024/276890-57-4.png)