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|Title:||Pathophysiological role of extrasynaptic GABAA receptors in typical absence epilepsy|
|Authors:||Di Giovanni, Giuseppe|
Errington, Adam C.
|Keywords:||GABA -- Receptors|
Petit mal epilepsy
|Publisher:||Malta Medical Journal|
|Citation:||Malta Medical Journal. 2011, Vol.23(3), p. 4-9|
|Abstract:||GABA 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.|
|Appears in Collections:||MMJ, Volume 23, Issue 3|
MMJ, Volume 23, Issue 3
Scholarly Works - FacM&SPB
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