GABAergic gain-of-function in absence seizures

Crunelli, Vincenzo ORCID: https://orcid.org/0000-0001-7154-9752, Leresche, Nathalie and Cope, David William 2010. GABAergic gain-of-function in absence seizures. Epilepsia 51 (S5) , p. 23. 10.1111/j.1528-1167.2010.02809.x

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Abstract

New evidence indicates that increased, rather than decreased, -aminobutyric acid (GABA)ergic inhibition characterizes typical absence seizures. In particular, enhanced tonic GABAA inhibition, resulting from a malfunction of the astrocytic GABA transporter GAT-1, occurs in thalamocortical neurons of all well-established pharmacologic and genetic models. Interestingly, GABAB receptors positively modulate this tonic current. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado-Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Biosciences Neuroscience and Mental Health Research Institute (NMHRI)
Subjects:	Q Science > Q Science (General)
Uncontrolled Keywords:	epilepsy; GABA B receptors; GAT-1; genetic models; initiation site; reticular thalamus; synchronous discharge; T-type calcium current
Additional Information:	Special Issue: Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition
Publisher:	Wiley
ISSN:	0013-9580
Last Modified:	19 Oct 2022 10:05
URI:	https://orca.cardiff.ac.uk/id/eprint/23168

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