Objective：In the present study, we determind whether status epilepticus or prolonged limbic seizures (induced by pilocarpine) altered GABAA receptor α1 subunit gene expression in the hippocampus. Methods: Status epilepticus was induced in male adult rats by a single i.p. injection of pilocarpine (320～340mg/kg). Rats that survived status epilepticus (definded as continous seizure activity in the EcoG for at least 40min) for 1h and 2h were sacrificed for G4BAA receptor gene expression and binding assay. In situ hybridization was used to measure regional mRNA levels, and ［3H］ flunitrazepam was used to label the benzodiazepine binding sites. Results: We found 2h after the onset of seizure, GABAA receptor α1 mRNA decresed significantly in the CA1 and CA3 fileds of hippocampus. No significant change in α1 mRNA was observed in the dentate gyrus. However, ［3H］ flunitrazepam binding decreased uniformly in CA1, CA3 and dentate gyrus 2h after status epileptius. 1h of continuous seizures did not produce any significant change in either α1 mRNA or ［3H］ flunitrazepam binding in any of the hippoceampal regions studied. Cresyl violet stained brain hippocampus areas 1h or 2h after the seizure-onset. Conclusion: These results suggest that status epilepticus-induced decreased GABAA receptor α1 gene expression and ［3H］ flunitrazepam biding in the hippocampus. The above changes make the brain more susceptibale for the development of chronic epilepsy.%目的：本实验研究大鼠癫痫持续状态动物模型的海马等部位GABAA受体α1亚单位基因表达和受体一配体结合的变化。方法：成年雄性大鼠经腹腔内注射320～340±5.87毫克/公斤毛果芸香碱(Pilocarpine)以制成癫痫持续状态动物模型，能在癫痫持续状态(定义为在皮质脑电图上显示痫性放电的至少40分钟的持续性痫性发作)下存活的大鼠在1小时和2小时后处于死，分别研究GABA受体基因表达和放射结合位点，用原位杂交方法来测定脑部mRNA水平，用［3H］flunirazepam标记GABAA受体benzodiazepam结合位点。结果：动物痫性发作2小时后海马的CA1和CA3区域GABAA受体α1亚单位mRNA显著下降，但是齿状回的α1 mRNA没有变化。［3H］flunirazepam标记受体-配体放射结合在持续2小时持续痫性发作后可见海马的CA1及CA3和齿状回中均见下降， 1小时的持续痫性发作尚未引起海马区域的任何α1 mRNA或［3H］flunirazepam受体-配体放射结合的任何改变，并用结晶染色1及2小时后的大脑海马部位。结论：本研究结果提示大鼠的癫痫持续状态可诱发海马区GABAA受体α1基因表达的改变和［3H］flinirazepam受体-配体结合的下降，上述改变可能使大脑更容易形成慢性癫痫病灶。
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