Gamma-hydroxybutyric acid-induced absence seizures in GluR2 null mutant mice.
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 to induce the absence seizures. We also tested the severity and duration of the seizure activity in this model. The results showed that the latency from GBL administration to onset of seizure was significantly prolonged in GluR2(-/-) mice when compared to GluR2(+/+) mice. The duration of spike-and-wave 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 baseline. These data suggest that the GluR2 subunit may be involved in the initiation and maintenance of absence seizures induced by GBL.[1]References
- Gamma-hydroxybutyric acid-induced absence seizures in GluR2 null mutant mice. Hu, R.Q., Cortez, M.A., Man, H.Y., Roder, J., Jia, Z., Wang, Y.T., Snead, O.C. Brain Res. (2001) [Pubmed]
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