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目的:观察大鼠颞叶癫痫发生后海马谷氨酸脱羧酶(glutamicaciddecar-boxylase,GAD)亚型GAD67蛋白的动态变化,探讨其意义和可能机制。方法:112只雄性SD大鼠随机分为实验组(n=70)与对照组(n=42),实验组大鼠选用海人酸腹腔注射法建立颞叶癫痫模型,对照组大鼠腹腔注射无菌生理盐水。选取腹腔注射后3,6,12,24,48h,7,30d为研究的时间点,颞叶海马的CA1区、CA3区、齿状回为研究部位。腹腔给药后每天观察大鼠的行为学变化,大鼠处死前进行脑电图描记。免疫组织化学法检测GAD67蛋白的表达。结果:海人酸致痫后6h实验组大鼠海马齿状回、CA3,CA1区的GAD67蛋白表达分别为0.60±0.02,0.61±0.02,0.58±0.02,致痫后24h分别为0.33±0.03,0.32±0.03,0.31±0.02,均较对照组(0.23±0.02,0.21±0.02,0.20±0.02)增高(P<0.05或0.01),6h时增高显著。结论:颞叶癫痫大鼠海马GAD67蛋白表达的增高是癫痫发生后机体的内源性抗痫机制之一。
OBJECTIVE: To observe the dynamic changes of GAD67 protein in hippocampal glutamate receptor subtype (GAD) in rat temporal lobe epilepsy and to explore its significance and possible mechanism. Methods: One hundred and twelve male Sprague-Dawley rats were randomly divided into experimental group (n = 70) and control group (n = 42). The rats in the experimental group were given intraperitoneal injection of kainic acid to establish the model of temporal lobe epilepsy. Sterile saline. At 3, 6, 12, 24, 48, 7 and 30 days after the intraperitoneal injection, the CA1, CA3 and dentate gyrus in the temporal lobe hippocampus were selected as the study sites. The behavior of rats was observed daily after intraperitoneal administration, and EEG was performed before the rats were sacrificed. Immunohistochemical detection of GAD67 protein expression. Results: The expression of GAD67 protein in hippocampal dentate gyrus, CA3 and CA1 area in experimental group was 0.60 ± 0.02, 0.61 ± 0.02 and 0.58 ± 0.02 respectively at 6 h after kainic acid-induced seizure, and was 0.33 ± 0.03 at 24h after epileptic seizure, 0.32 ± 0.03,0.31 ± 0.02, which were significantly higher than that of the control group (0.23 ± 0.02,0.21 ± 0.02,0.20 ± 0.02) (P <0.05 or 0.01). Conclusion: The increased expression of GAD67 in the hippocampus of temporal lobe epilepsy rats is one of the mechanisms of endogenous anti-epilepsy after epilepsy.