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dc.contributor.authorDi Giovanni, Giuseppe-
dc.contributor.authorErrington, Adam C.-
dc.contributor.authorCrunelli, Vincenzo-
dc.date.accessioned2015-01-30T10:53:47Z-
dc.date.available2015-01-30T10:53:47Z-
dc.date.issued2011-
dc.identifier.citationMalta Medical Journal. 2011, Vol.23(3), p. 4-9en_GB
dc.identifier.urihttps://www.um.edu.mt/library/oar//handle/123456789/1060-
dc.description.abstractGABA is the principal inhibitory neurotransmitter in the mammalian CNS. It acts via two classes of receptors, the GABAA, a ligand gated ion channel (ionotropic receptor) and the metabotropic G-protein coupled GABAB receptor. While synaptic GABAA receptors underlie classical ‘phasic’ GABAA receptor-mediated inhibition, extrasynaptic GABAA receptors (eGABAAR) mediate a new form of inhibition, termed ‘tonic’ GABAA inhibition. The subunit composition of eGABAARs differs from those present at the synapse, resulting in pharmacologically and functionally distinct properties. In this mini-review the findings presented at the 2nd Neuroscience Day meeting held last July in Malta will be summarised. Particular emphasis will be given to the important pathophysiological role of eGABAAR within thalamocortical circuits as a major player in nonconvulsive absence epilepsy. The new findings presented at the conference suggest that enhanced tonic inhibition is a common cause of seizures in several animal models of absence epilepsy and may provide new targets for therapeutic intervention.en_GB
dc.language.isoenen_GB
dc.publisherMalta Medical Journalen_GB
dc.rightsinfo:eu-repo/semantics/openAccessen_GB
dc.subjectGABA -- Receptorsen_GB
dc.subjectPetit mal epilepsyen_GB
dc.titlePathophysiological role of extrasynaptic GABAA receptors in typical absence epilepsyen_GB
dc.typearticleen_GB
dc.rights.holderThe copyright of this work belongs to the author(s)/publisher. The rights of this work are as defined by the appropriate Copyright Legislation or as modified by any successive legislation. Users may access this work and can make use of the information contained in accordance with the Copyright Legislation provided that the author must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the prior permission of the copyright holder.en_GB
dc.description.reviewedpeer-reviewed-
Appears in Collections:MMJ, Volume 23, Issue 3
MMJ, Volume 23, Issue 3
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