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损伤性癫痫模型大鼠海马和额叶突触蛋白的动态表达 被引量:3

Time course of cortical and hippocampal synaptophysin expression changes in rats with posttraumatic epilepsy induced by intracortical FeCl2 injection
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摘要 目的通过观察FeCl2皮层注射致损伤性癫痫(PTE)模型大鼠海马、额叶突触蛋白P38的表达变化.探讨突触可塑性在PTE发病机制中的作用。方法健康成年雄性SD大鼠采用随机数字表法分为正常对照组(n=5)、假手术组(n=12)、模型组(n=20),采取立体定向皮层注射FeCl2(0.1moL/L,10μL)建立PTE模型,假手术组注入等量生理盐水,正常对照组不做处理。观察各组大鼠EEG的变化并应用免疫组织化学方法检测大鼠造模后不同时间点(1h、7d、14d、30d)海马、额叶P38的表达。结果大多数模型组大鼠在注射FeCl2后不久记录到癫痫样放电;与假手术组比较,模型组不同时间点右侧额叶P38表达减少,差异有统计学意义(P〈0.05);与正常对照组和假手术组比较,致痫1h后,CA3区多形层、辐射层、腔隙层和齿状回(DG)分子层P38表达均无明显变化,7d后P38表达增加,维持到30d,差异均有统计学意义(P〈0.05)。结论与突触蛋白P38表达相关的突触可塑性变化在PTE的发病机制中可能起重要作用。 Objective To observe the time course of changes in synaptophysin (P38) expression in the cortex and hippocampus of rats with posttraumatic epilepsy (PTE), and explore the role of synaptie plasticity in the epileptogenesis of PTE. Methods Thirty-seven male Sprague-Dawley rats were randomized into normal control group (n=5), sham-operated group (n=12) with intracortical saline injection, and PTE model group (n=20) with stereotactic FeC12 injection (0.1 mol/L, 10 tL1) into the motor cortex. The expression of P38 in the brain cortex and hippoeampus of the rats was detected immunohistochemically at 1 h and 7, 14 and 30 days after the injections. Results Most of the rats with FeCl2 injection developed isolated epileptiform discharges soon after the injection. Compared with the sham-operated groups, the rats in PTE group showed significantly decreased P38 expression in the right frontal cortex at all the time points of measurement (P〈0.05). At 1 h after FeCl2 injection, P38 expression in the polymorphic layer, stratum lacunosum and stratum radiatum of the right hippocampal CA3 area and DG molecular layer underwent no significant changes (P〉0.05), but at 7 days, the expression increased significantly in all the stratum regions of the right hippocampal CA3 area, and this high expression level was maintained till 30 days after the injection. Conclusion Synaptic plasticity alterations in relation to P38 expression changes in the cortex and hippocampus may play an important role in the epileptogenesis of PTE in this rat model.
出处 《中华神经医学杂志》 CAS CSCD 北大核心 2009年第6期551-555,共5页 Chinese Journal of Neuromedicine
基金 福建省科技计划项目(2007F5045) 福建省高校新世纪人才支持计划(NCETFJ-0702)
关键词 损伤性癫痫 氯化亚铁 突触蛋白 突触可塑性 Posttraumatic Epilepsy Ferrous chloride Synaptophysin Synaptic plasticity
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