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目的探讨脑梗死早期亚临床发作的病理生理机制。方法采用线栓法制作大鼠右侧大脑中动脉阻塞(MCAO)模型,监测大鼠脑电活动,检测海马组织中胶质谷氨酸转运体-1(GLT-1)的表达。结果大鼠脑梗死后样放电的发生率为27·4%,亚临床发作组海马CA1区和CA3区GLT-1免疫表达[分别为(344·5±35·0)μm2和(360·4±13·5)μm2]显著低于非亚临床发作组[CA1区和CA3区分别为(447·0±22·8)μm2和(402·3±28·5)μm2],而两组GLT-1在齿状回表达差异无统计学意义。结论大鼠脑梗死后可出现样放电,并与海马组织中CA1区和CA3区GLT-1表达下调有关。
Objective To explore the pathophysiological mechanism of subclinical seizure in early stage of cerebral infarction. Methods The right middle cerebral artery occlusion (MCAO) model was established by thread occlusion. EEG activity was measured in rats. The expression of glial glutamate transporter-1 (GLT-1) in hippocampus was detected. Results The incidence of pulsatile discharge after cerebral infarction in rats was 27.4%. Immunohistochemical expression of GLT-1 in hippocampal CA1 and CA3 of the subclinical group [(344.5 ± 35.0) μm2 and (360 · 4 ± 13 · 5) μm 2] were significantly lower than those in the non-subclinical seizure group (447 · 0 ± 22 · 8 μm 2 and (402 · 3 ± 28 · 5) μm 2 in CA1 and CA3, respectively) There was no significant difference in the expression of GLT-1 in the dentate gyrus. Conclusion Sini-like discharge may occur after cerebral infarction in rats and is related to the down-regulation of GLT-1 expression in CA1 and CA3 in hippocampus.