Augmentation of Tonic GABAA Inhibition in Absence Epilepsy Therapeutic Value of Inverse Agonists at Extrasynaptic GABAA Receptors英文文献资料.docVIP

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Augmentation of Tonic GABAA Inhibition in Absence Epilepsy Therapeutic Value of Inverse Agonists at Extrasynaptic GABAA Receptors英文文献资料.doc

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Augmentation of Tonic GABAA Inhibition in Absence Epilepsy Therapeutic Value of Inverse Agonists at Extrasynaptic GABAA Receptors英文文献资料

HindawiPublishingCorporation AdvancesinPharmacologicalSciences Volume2011,ArticleID790590,12pages doi:10.1155/2011/790590 ReviewArticle AugmentationofTonicGABAAInhibitionin AbsenceEpilepsy:TherapeuticValueofInverse AgonistsatExtrasynapticGABAAReceptors andVincenzoCrunelli AdamC.Errington,1,2DavidW.Cope,1 1 1 2 SchoolofBiosciences,Cardi?University,MuseumAvenue,Cardi?CF103US,UK NeuroscienceDivision,SchoolofBiosciences,Cardi?University,MuseumAvenue,Cardi?CF103AX,UK CorrespondenceshouldbeaddressedtoAdamC.Errington,erringtonac@cardi?.ac.uk Received17March2011;Accepted16May2011 AcademicEditor:KeithWa?ord Copyright?2011AdamC.Erringtonetal.ThisisanopenaccessarticledistributedundertheCreativeCommonsAttribution License,whichpermitsunrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalworkisproperly cited. It is well established that impaired GABAergic inhibition within neuronal networks can lead to hypersynchronous ?ring patterns that are the typical cellular hallmark of convulsive epileptic seizures. However, recent ?ndings have highlighted that apathologicalenhancementofGABAergicsignallingwithinthalamocorticalcircuitsisanecessaryandsu?cientconditionfor nonconvulsivetypicalabsenceseizuregenesis.Inparticular,increasedactivationofextrasynapticGABAAreceptors(eGABAAR) andaugmented“tonic”GABAA inhibitioninthalamocorticalneuronshavebeendemonstratedacrossarangeofgeneticand pharmacologicalmodelsofabsenceepilepsy.Moreover,evidencefrommonogenicmousemodels(stargazer/lethargic)andthe polygenicGeneticAbsenceEpilepsyRatsfromStrasbourg(GAERS)indicatethatthemechanismunderlyingeGABAARgainof functionisnonneuronalinnatureandresultsfromade?ciencyinastrocyticGABAuptakethroughtheGAT-1transporter.These resultschallengetheexistingtheorythattypicalabsenceseizuresareunderpinnedbyawidespreadlossofGABAergicfunction inthalamocorticalcircuitsandillustrateavitalroleforastrocytesinthepathologyoftypicalabsenceepilepsy.Moreover,they explainwhypharmacologicala