augmentation of tonic gabaa inhibition in absence epilepsy therapeutic value of inverse agonists at extrasynaptic gabaa receptors增加失神癫痫治疗价值的滋补gabaa抑制逆gabaa受体受体激动剂在extrasynaptic.pdfVIP

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augmentation of tonic gabaa inhibition in absence epilepsy therapeutic value of inverse agonists at extrasynaptic gabaa receptors增加失神癫痫治疗价值的滋补gabaa抑制逆gabaa受体受体激动剂在extrasynaptic.pdf

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augmentation of tonic gabaa inhibition in absence epilepsy therapeutic value of inverse agonists at extrasynaptic gabaa receptors增加失神癫痫治疗价值的滋补gabaa抑制逆gabaa受体受体激动剂在extrasynaptic

Hindawi Publishing Corporation Advances in Pharmacological Sciences Volume 2011, Article ID 790590, 12 pages doi:10.1155/2011/790590 Review Article Augmentation of Tonic GABAA Inhibition in Absence Epilepsy: Therapeutic Value of Inverse Agonists at Extrasynaptic GABAA Receptors Adam C. Errington,1, 2 David W. Cope,1 and Vincenzo Crunelli1 1 School of Biosciences, Cardiﬀ University, Museum Avenue, Cardiﬀ CF10 3US, UK 2 Neuroscience Division, School of Biosciences, Cardiﬀ University, Museum Avenue, Cardiﬀ CF10 3AX, UK Correspondence should be addressed to Adam C. Errington, erringtonac@cardiﬀ.ac.uk Received 17 March 2011; Accepted 16 May 2011 Academic Editor: Keith Waﬀord Copyright © 2011 Adam C. Errington et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. It is well established that impaired GABAergic inhibition within neuronal networks can lead to hypersynchronous ﬁring patterns that are the typical cellular hallmark of convulsive epileptic seizures. However, recent ﬁndings have highlighted that a pathological enhancement of GABAergic signalling within thalamocortical circuits is a necessary and suﬃcient condition for nonconvulsive typical absence seizure genesis. In particular, increased activation of extrasynaptic GABA receptors (eGABA R) A A and augmented “tonic” GABAA inhibition in thalamocortical neurons have been demonstrated across a range of genetic and pharmacological models of absence epilepsy. Moreover, evidence from monoge