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Transition to absence seizures and the role of GABAA receptors

Crunelli, Vincenzo, Cope, David William and Terry, John R. 2011. Transition to absence seizures and the role of GABAA receptors. Epilepsy Research 97 (3) , pp. 283-289. 10.1016/j.eplepsyres.2011.07.011

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Abstract

Absence seizures appear to be initiated in a putative cortical ‘initiation site’ by the expression of medium-amplitude 5-9Hz oscillations, that may in part be due to a decreased phasic GABAA receptor function. These oscillations rapidly spread to other cortical areas and to the thalamus, leading to fully developed generalized spike and wave discharges. In thalamocortical neurons of genetic models, phasic GABAA inhibition is either unchanged or increased, whereas tonic GABAA inhibition is increased both in genetic and pharmacological models. This enhanced tonic inhibition is required for absence seizure generation, and in genetic models it results from a malfunction in the astrocytic GABA transporter GAT-1. Contradictory results from inbred and transgenic animals still do not allow us to draw firm conclusions on changes in phasic GABAA inhibition in the GABAergic neurons of the nucleus reticularis thalami. Mathematical modelling may enhance our understanding of these competing hypotheses, by permitting investigations of their mechanistic aspects, hence enabling a greater understanding of the processes underlying seizure generation and evolution.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Biosciences
Neuroscience and Mental Health Research Institute (NMHRI)
Subjects: R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
Uncontrolled Keywords: phasic GABAA inhibition; tonic GABAA inhibition; GABAB receptors; GHB; GAERS; mathematical modelling
Publisher: Elsevier
ISSN: 0920-1211
Related URLs:
Last Modified: 04 Jun 2017 03:21
URI: http://orca.cf.ac.uk/id/eprint/20034

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