Physiopathology of kainate receptors in epilepsy.
Current Opinion in Pharmacology. 2015-02-01; 20: 83-88
DOI: 10.1016/j.coph.2014.11.012
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1. Curr Opin Pharmacol. 2015 Feb;20:83-8. doi: 10.1016/j.coph.2014.11.012. Epub 2014
Dec 13.
Physiopathology of kainate receptors in epilepsy.
Crépel V(1), Mulle C(2).
Author information:
(1)INSERM, INMED, U901, 13009 Marseille, France; Aix-Marseille Université, UMR
901, 13009 Marseille, France.
(2)Interdisciplinary Institute for Neuroscience, CNRS UMR 5297, France;
University of Bordeaux, F-33000 Bordeaux, France. Electronic address:
.
Kainate receptors (KARs) are tetrameric ionotropic glutamate receptors composed
of the combinations of five subunits GluK1-GluK5. KARs are structurally related
to AMPA receptors but they serve quite distinct functions by regulating the
activity of synaptic circuits at presynaptic and postsynaptic sites, through
either ionotropic or metabotropic actions. Although kainate is a potent
neurotoxin known to induce acute seizures through activation of KARs, the actual
role of KARs in the clinically-relevant chronic phase of temporal lobe epilepsy
(TLE) has long been elusive. Recent evidences have described pathophysiological
mechanisms of heteromeric GluK2/GluK5 KARs in generating recurrent seizures in
chronic epilepsy. The role of the other major subunit GluK1 in epileptogenic
activity is still a matter of debate. This review will present the current
knowledge on the subtype-specific pharmacology of KARs and highlight recent
results linking KARs to epileptic conditions.
Copyright © 2014 Elsevier Ltd. All rights reserved.
DOI: 10.1016/j.coph.2014.11.012
PMID: 25506747 [Indexed for MEDLINE]