OBJECTIVE: In the present study, we determinded whether status epilepticus or prolonged limbic seizures ( induced by pilocarpine) altered GABA A receptor αl subunit gene expression m the hippocanpus. BACKGROUND: A decrease in GABAergic inhibition during epileptogenesis plays an imprortant role in the development of persistent hyperexcitability observed during chronic epilepsy. METHODS: Stares epilepticus was reduced in male adult rats by a single i.p. injection ofpilocarpine (320-340 mg/kg). Rats that survived status epilepticus ( definded as continous seizure activity in the EcoG for at least 40 min) for 1 h and 2 h were sacrificed for GABA A receptor gene expression and binding assay. In situ hybridization was used to measure regional mRNA levels, and [3H] flunirazepam used to label the benzodiazepine binding sites. RESULTS: We found that 2h after the onset of seizure, GABA A receptor α1 m RNA decresed significarntly in the CA1 and CA3 fields of hippocampus. No significant change in ctl mRNA was observed in the dentate gyrus. However, [3H] flunirazepam binding decreased uniformly in CA l, CA3 and dentate gyrus 2h after status epfileptius. 1 h ofcontinuous seizures did not produce any significant change in either αl mRNA or [3H] flunirazepam birding in any of the hippocampal regions studied. Cresyl violet staining of the brain hippocampus areas lh or 2h after the seizure-onset. DISCUSSION: The above changes make the brain more susceptible for the development of chronic epilepsy. CONCLUSION: These results suggest that status epilepticus-induced decreased in GABA A recepor αl gene expression and [3H] flunirazepam binding in the hippocampus.
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