目的：γ-氨基丁酸A受体（GABAAR）作为脑内最重要的抑制性受体在脑功能中起重要作用。该实验通过研究新生期反复惊厥对大鼠脑内GABAAR α1和β2亚单位表达的短期影响，探讨其与发育中脑损伤的关系。方法：生后7 d的Sprague-Dawley大鼠随机分成两组，每组32只，惊厥组每日吸入三氟乙醚诱导惊厥发作1 次，每次持续30 min，连续6 d；对照组同样操作但不吸入三氟乙醚。分别于反复惊厥后1 d和7 d每组各处死16只大鼠，每个时间点分别采用免疫组化方法和Western blot方法观察大鼠大脑皮层及海马GABAAR α1和β2亚单位表达的变化。结果：反复惊厥后1 d时，在惊厥组大鼠顶叶及海马齿状核、CA3和CA4区GABAAR α1亚单位免疫化学累积光密度（AOD）较对照组明显增高（P＜0.05），反复惊厥后7 d时，在惊厥组大鼠顶叶及海马齿状核、CA1至CA4区GABAAR α1亚单位免疫化学AOD较对照组明显增高（P＜0.05），反复惊厥后1 d和7 d时，在惊厥组大鼠大脑皮层和海马区GABAAR α1亚单位蛋白表达均明显高于对照组（P＜0.01）。反复惊厥后7 d时，在惊厥组大鼠海马CA1、CA2区GABAAR β2亚单位免疫化学AOD明显高于对照组（P<0.05），在丘脑区明显低于对照组（P<0.05），惊厥组大鼠海马区GABAAR β2亚单位蛋白表达明显高于对照组（P<0.05）。结论:新生大鼠反复惊厥造成脑内GABAAR α1和β2亚单位表达的短期改变，这种改变可能参与发育期惊厥性脑损伤。

OBJECTIVE: To investigate the short-term effects of flurothyl-induced neonatal recurrent seizures on γ-aminobutyric acid A receptor (GABAAR) α1 and β2 subunit expression in the rat brain, and to study the relationship between the alterations of GABAAR subunits in the developing brain and seizure-induced brain injury.METHODS: Sixty-four 7-day-old Sprague-Dawley rats were randomly divided into two groups: control and seizure. Seizures were induced by inhalant flurothyl daily for six consecutive days. The expression of GABAAR α1 and β2 subunits protein in the cerebral cortex and the hippocampus were detected by Western blot and immunohistochemistry method 1 and 7 days after recurrent seizures.RESULTS: Compared to the control, the accumulated optical density (AOD) of GABAAR α1 subunit immunoreactivity (IR) in the parietal cortex, the CA3-CA4 regions and the dentate gyrus in seizure rats increased significantly 1 day after recurrent seizures (P<0.05). The AOD of GABAAR α1 subunit IR in the parietal cortex, the CA1-CA4 regions and the dentate gyrus in seizure rats increased significantly 7 days after recurrent seizures compared with the control (P<0.05). The expression of GABAAR α1 subunit in the hippicampus and the cerebral cortex increased significantly in seizure rats compared with that in control rats 1 and 7 days after recurrent seizures. After 7 days of recurrent seizures, the AOD of GABAAR β2 subunit IR in the CA1-CA2 regions increased significantly in the seizure group compared with that in the control group (P<0.05), but the AOD of GABAAR β2 subunit IR in the thalamus decreased significantly in the seizure group compared with that in the control group (P<0.05). The expression of GABAAR β2 subunit protein in the hippocampus increased significantly in the seizure group compared with that in the control group 7 days after recurrent seizures (P<0.05). CONCLUSIONS: Recurrent neonatal seizures may result in the short-term alterations of GABAAR α1 and β2 subunits expression in the cerebral cortex and the hippocampus in rats, suggesting the alterations of GABAAR subunit expression may be related to the developing brain injury following recurrent seizures.