摘要
目的 探讨GAD6 7/GAD6 5在颞叶癫痫发生后大鼠海马内源性促痫机制中的作用。方法 112只雄性SD大鼠随机分为实验组 (n =70 )与对照组 (n =4 2 ) ,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 3h、6h、12h、2 4h、4 8h、7d、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EEG描记。免疫组织化学法检测GAD6 5、GAD6 7蛋白的表达。结果 海人酸致痫后 6h ,实验组大鼠海马CA1区、CA3区GAD6 7/GAD6 5的比率较对照组升高 (P <0 .0 1) ;海人酸致痫后 30d ,实验组大鼠海马齿状回GAD6 7/GAD6 5的比率较对照组降低 (P <0 .0 5 )。结论 颞叶癫痫急性期CA1区、CA3区GAD6 7/GAD6 5比率的增高及慢性期齿状回GAD6 7/GAD6
Objective To discuss the effect of GAD67/GAD65 on endogenous self acceleration mechanism in hippocampus after seizures.Methods Epileptic rats were injected with kainate intraperitoneally to establish temporal lobe epilepsy model,and the controls were injected with saline instead of kainate. At 3 h,6 h,12 h,24 h,48 h and 7 d, 30 d after kainate injection, the rats in two groups were anaesthetized and perfused and EEGs were recorded antemortem.By use of immunohistochemistry, the GAD65 and GAD67 protein was analyzed at different time quantitatively in the dentate gyrus,CA1 and CA3 regions of hippocampus.Results The GAD67/GAD65 ratio increased at 6 h in CA1 and CA3 regions following the onset of seizure and decreased at 30 days in dentate gryus.Conclusions The up regulation of GAD67/GAD65 ratio in CA1 and CA3 regions in acute temporal lobe epilepsy and the low regulation of GAD67/GAD65 ratio in dentate gryus of chronic temporal lobe epilepsy could be the important factors in the occurrence of epilepsy and the self protection mechanism after seizures.
出处
《卒中与神经疾病》
2004年第5期279-282,共4页
Stroke and Nervous Diseases