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GABAA受体γ2亚单位在海人酸颞叶癫痫大鼠海马内的表达 被引量:2

Expression of GABAA Receptor γ2 Subunit in Hippocampus of Rats with KA-induced Temporal Lobe Epilepsy
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摘要 目的:探讨癫痫发作后GABAA受体γ2亚单位在海马各区的动态表达以及氯硝西泮干预对其表达的影响。方法:健康成年雄性SD大鼠40只,随机分为对照组5只,致痫组15只,干预组15只,干预对照组5只。大鼠海马CA3区注射海人酸建立颞叶癫痫模型,干预组大鼠在致痫前予以氯硝西泮灌胃。于致痫后6 h、12 h和1 d采用免疫组化法检测各组大鼠海马CA1及CA3区γ-氨基丁酸A受体γ2亚单位(GABAARγ2)的动态表达水平。结果:致痫组在海人酸给药后6 h、12 h及1 d,海马CA3区GABAARγ2蛋白表达均显著低于对照组(P<0.01);CA1区GABAARγ2蛋白表达也下降,注射后1 d显著低于对照组(P<0.01)。干预组在海人酸注射后1 d CA1和CA3区GABAARγ2蛋白表达低于对照组(P<0.05);海人酸注射后6 h、12 h及1 d,CA3区GABAARγ2蛋白表达均高于同时间点致痫组(P<0.05),CA1区于海人酸注射后1 d,GABAARγ2蛋白表达显著高于同时间点致痫组(P<0.01)。结论:海人酸诱导的颞叶癫痫模型中,海马GABAARγ2蛋白表达减少,氯硝西泮可缓解颞叶癫痫导致的GABAARγ2蛋白表达减少。 Objective: To study the expression of GABAA receptor γ2 subunit(GABAARγ2) protein in hippocampus of rats with KA-induced temporal lobe epilepsy. To investigate the effect of clonazepam(CZP) administration on expression of GABAARγ2. Methods: Forty male SD rats were randomly divided into control group(n=5),epilepsy group(n=15), intervention group(n=15), and intervention control group(n=5). Temporal lobe epilepsy model was established by injecting kainic acid into CA3 region of the hippocampus in rats in both the epilepsy and intervention groups. Rats in the intervention group were treated with CZP. The expression of GABAARγ2 protein was investigated by immunohistochemistry at 6 h, 12 h and 1 d after operation respectively. Results: The expression of GABAARγ2 protein in CA3 of the rats in the epilepsy group was significantly lower than that in the control group(P〈0.01) at 6 h, 12 h and 1 d after operation and the expression of GABAARγ2 protein in CA1 region was significantly lower than that in the control group(P〈0.01) only at 1 d after operation. The expression of GABAARγ2 protein in both CA3 and CA1 regions in the intervention group were lower than that in the control group(P〈0.05). The expression of GABAARγ2 protein in CA3 region was significantly higher than that in the epilepsy group at 6 h, 12 h and 1 d after operation(P〈0.05) and the expression of GABAARγ2 protein in CA1 was significantly higher than that in the epilepsy group(P〈0.01) only at 1 d after operation. Conclusion: The expression of GABAARγ2 protein was decreased in hippocampus of temporal lobe epilepsy model rats, and CZP could relieve the decrease of GABAARγ2 protein.
出处 《神经损伤与功能重建》 2015年第2期110-112,共3页 Neural Injury and Functional Reconstruction
基金 江苏省自然科学基金(No.BK2011309)
关键词 颞叶癫痫 GABAA受体 γ2亚单位 海人酸 海马 temporal lobe epilepsy GABAA receptor γ2 subunit kainic acid hippocampus
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