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.