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Ethanol Augments GABAergic Transmission in the Central Amygdala via CRF1 Receptors
Zhiguo Nie,1Paul Schweitzer,1Amanda J. Roberts,1Samuel G. Madamba,1Scott D. Moore,2George Robert Siggins1*
The central amygdala (CeA) plays a role in the relationshipamong stress, corticotropin-releasing factor (CRF), and alcoholabuse. In whole-cell recordings, both CRF and ethanol enhanced-aminobutyric acid–mediated (GABAergic) neurotransmissionin CeA neurons from wild-type and CRF2 receptor knockout mice,but not CRF1 receptor knockout mice. CRF1 (but not CRF2) receptorantagonists blocked both CRF and ethanol effects in wild-typemice. These data indicate that CRF1 receptors mediate ethanolenhancement of GABAergic synaptic transmission in the CeA, andthey suggest a cellular mechanism underlying involvement ofCRF in ethanol's behavioral and motivational effects.
1 Department of Neuropharmacology and Alcohol Research Center, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. 2 Department of Psychiatry, Duke University, Durham, NC 27710, USA.
* To whom correspondence should be addressed. E-mail: geobob{at}scripps.edu
Protein kinase C epsilon mediation of CRF- and ethanol-induced GABA release in central amygdala.
M. Bajo, M. T. Cruz, G. R. Siggins, R. Messing, and M. Roberto (2008)
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105, 8410-8415
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Presynaptic {delta} Opioid Receptors Regulate Ethanol Actions in Central Amygdala.
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J. Pharmacol. Exp. Ther.
320, 917-925
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Involvement of Non-NMDA Glutamate Receptors in Central Amygdala in Synaptic Actions of Ethanol and Ethanol-Induced Reward Behavior.
Long-Term Potentiation (LTP) in the Central Amygdala (CeA) Is Enhanced After Prolonged Withdrawal From Chronic Cocaine and Requires CRF1 Receptors.
Y. Fu, S. Pollandt, J. Liu, B. Krishnan, K. Genzer, L. Orozco-Cabal, J. P. Gallagher, and P. Shinnick-Gallagher (2007)
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Corticotropin-Releasing Factor within the Central Nucleus of the Amygdala Mediates Enhanced Ethanol Self-Administration in Withdrawn, Ethanol-Dependent Rats..
C. K. Funk, L. E. O'Dell, E. F. Crawford, and G. F. Koob (2006)
J. Neurosci.
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Ethanol Potentiates GABAergic Synaptic Transmission in a Postsynaptic Neuron/Synaptic Bouton Preparation From Basolateral Amygdala.
-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. 
