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.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Alcohol Drinking
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Amygdala / drug effects
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Amygdala / physiology*
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Animals
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Corticotropin-Releasing Hormone / pharmacology
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Dose-Response Relationship, Drug
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Ethanol / pharmacology*
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Evoked Potentials / drug effects
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Neurons / drug effects
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Neurons / physiology*
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Patch-Clamp Techniques
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Receptors, Corticotropin-Releasing Hormone / antagonists & inhibitors
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Receptors, Corticotropin-Releasing Hormone / genetics
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Receptors, Corticotropin-Releasing Hormone / metabolism*
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Receptors, GABA-A / metabolism
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Stress, Psychological / physiopathology
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Synaptic Transmission / drug effects*
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gamma-Aminobutyric Acid / metabolism*
Substances
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CRF receptor type 2
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Receptors, Corticotropin-Releasing Hormone
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Receptors, GABA-A
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Ethanol
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gamma-Aminobutyric Acid
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CRF receptor type 1
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Corticotropin-Releasing Hormone