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The Journal of Neuroscience, October 14, 2009, 29(41):12757-12763; doi:10.1523/JNEUROSCI.3340-09.2009

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Symposia and Mini-Symposia
Extrasynaptic GABAA Receptors: Form, Pharmacology, and Function

Delia Belelli,1 Neil L. Harrison,2 Jamie Maguire,3 Robert L. Macdonald,4,5,6 Matthew C. Walker,7 and David W. Cope8

1Division of Medical Sciences, Centre for Neuroscience, University of Dundee, Ninewells Hospital and Medical School, Dundee DD1 9SY, United Kingdom, 2Department of Anesthesiology, Columbia University, New York, New York 10032-3784, 3Department of Neurology, University of California, Los Angeles, Los Angeles, California 90095-73352, 4Departments of Neurology, 5Molecular Physiology and Biophysics, and 6Pharmacology, Vanderbilt University, Nashville, Tennessee 37212, 7Institute of Neurology, University College London, London WC1N 2BG, United Kingdom, and 8School of Biosciences, Cardiff University, Cardiff CF10 3AX, United Kingdom

Correspondence should be addressed to David W. Cope, School of Biosciences, Cardiff University, Museum Avenue, Cardiff CF10 3AX, UK. Email: copedw{at}cf.ac.uk

GABA is the principal inhibitory neurotransmitter in the CNS and acts via GABAA and GABAB receptors. Recently, a novel form of GABAA receptor-mediated inhibition, termed "tonic" inhibition, has been described. Whereas synaptic GABAA receptors underlie classical "phasic" GABAA receptor-mediated inhibition (inhibitory postsynaptic currents), tonic GABAA receptor-mediated inhibition results from the activation of extrasynaptic receptors by low concentrations of ambient GABA. Extrasynaptic GABAA receptors are composed of receptor subunits that convey biophysical properties ideally suited to the generation of persistent inhibition and are pharmacologically and functionally distinct from their synaptic counterparts. This mini-symposium review highlights ongoing work examining the properties of recombinant and native extrasynaptic GABAA receptors and their preferential targeting by endogenous and clinically relevant agents. In addition, it emphasizes the important role of extrasynaptic GABAA receptors in GABAergic inhibition throughout the CNS and identifies them as a major player in both physiological and pathophysiological processes.

Received July 13, 2009; revised Aug. 20, 2009; accepted Aug. 21, 2009.

Correspondence should be addressed to David W. Cope, School of Biosciences, Cardiff University, Museum Avenue, Cardiff CF10 3AX, UK. Email: copedw{at}cf.ac.uk






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