Abstract
Administration of γ-butyrolactone (GBL) induced absence-like seizures accompanied by 6-Hz spike and wave discharges (SWDs) in mice. GBL also increased nuclear CRE- and AP-1 DNA-binding activities significantly in the thalamus + midbrain and cerebral cortex but not in other regions of brain. CGP 35348, a GABAB antagonist, suppressed GBL-induced absence seizure behavior, SWDs and nuclear CRE- and AP-1 DNA-binding activities. These results suggest that GABAB receptor-mediated synaptic responses are involved in GBL-induced absence-like seizures and that the increases in nuclear CRE- and AP-1 DNA-binding activities are correlated with the seizures.
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