gamma-hydroxybutyric acid-induced absence seizures in GluR2 null mutant mice

Citation
Rq. Hu et al., gamma-hydroxybutyric acid-induced absence seizures in GluR2 null mutant mice, BRAIN RES, 897(1-2), 2001, pp. 27-35
Citations number
35
Categorie Soggetti
Neurosciences & Behavoir
Journal title
BRAIN RESEARCH
ISSN journal
00068993 → ACNP
Volume
897
Issue
1-2
Year of publication
2001
Pages
27 - 35
Database
ISI
SICI code
0006-8993(20010406)897:1-2<27:GAASIG>2.0.ZU;2-Y
Abstract
In this electrophysiological study, we examined the susceptibility of GluR2 mutant null mice to absence seizures in comparison with wild-type controls . The prodrug of (GHB), gamma -butyrolactone (GBL) was given systemically t o induce the absence seizures. We also tested the severity and duration of the seizure activity in this model. The results showed that the latency fro m GBL administration to onset of seizure was significantly prolonged in Glu R2(-/-) mice when compared to GluR2(+/+) mice. The duration of spike-and-wa ve discharges (SWD) was also significantly decreased in the GluR2(-/-) mice . Ninety minutes following GBL administration, wild-type animals continued to exhibit intermittent SWD bursts while GluR2(-/-) mice had returned to ba seline. These data suggest that the GluR2 subunit may be involved in the in itiation and maintenance of absence seizures induced by GBL. (C) 2001 Elsev ier Science B.V. All rights reserved.