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Published online on February 3, 2003, 10.1073/pnas.0437926100
PNAS | February 18, 2003 | vol. 100 | no. 4 | 2053-2058


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Neuroscience
 Ethanol increases GABAergic transmission at both pre- and postsynaptic sites in rat central amygdala neurons

(alcohol|GABA IPSP/Cs|paired-pulse facilitation|miniature synaptic current|electrophysiology)

Marisa Roberto*, Samuel G. Madamba*, Scott D. Mooredagger , Melanie K. Tallent*,Dagger , and George R. Siggins*,§

* Department of Neuropharmacology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037; dagger  Department of Psychiatry, Duke University, Durham, NC 27710; and Dagger  Department of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, PA 19102

Communicated by Floyd E. Bloom, The Scripps Research Institute, La Jolla, CA, December 24, 2002 (received for review October 23, 2002)

We examined the interaction of ethanol with the gamma -aminobutyric acid (GABA)ergic system in neurons of slices of the rat central amygdala nucleus (CeA), a brain region thought to be critical for the reinforcing effects of ethanol. Brief superfusion of 11-66 mM ethanol significantly increased GABA type A (GABAA) receptor-mediated inhibitory postsynaptic potentials (IPSPs) and currents (IPSCs) in most CeA neurons, with a low apparent EC50 of 20 mM. Acute superfusion of 44 mM ethanol increased the amplitude of evoked GABAA IPSPs and IPSCs in 70% of CeA neurons. The ethanol enhancement of IPSPs and IPSCs occurred to a similar extent in the presence of the GABA type B (GABAB) receptor antagonist CGP 55845A, suggesting that this receptor is not involved in the ethanol effect on CeA neurons. Ethanol superfusion also decreased paired-pulse facilitation of evoked GABAA IPSPs and IPSCs and always increased the frequency and sometimes the amplitude of spontaneous miniature GABAA IPSCs as well as responses to local GABA application, indicating both presynaptic and postsynaptic sites of action for ethanol. Thus, the CeA is the first brain region to reveal, without conditional treatments such as GABAB antagonists, consistent, low-dose ethanol enhancement of GABAergic transmission at both pre- and postsynaptic sites. These findings add further support to the contention that the ethanol-GABA interaction in CeA plays an important role in the reinforcing effects of ethanol.

§ To whom correspondence should be addressed at: CVN-12, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037. E-mail: geobob{at}scripps.edu.

www.pnas.org/cgi/doi/10.1073/pnas.0437926100
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