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实验性大脑皮层梗死后中枢神经系统相关部位的神经可塑性
引用本文:曾进胜,李华,范玉华,余剑,陈向燕,洪华,陶玉倩,黄如训. 实验性大脑皮层梗死后中枢神经系统相关部位的神经可塑性[J]. 中国康复医学杂志, 2002, 17(2): 69-71
作者姓名:曾进胜  李华  范玉华  余剑  陈向燕  洪华  陶玉倩  黄如训
作者单位:1. 中山大学附属第一医院神经脑血管科,广州,510080
2. 深圳市第二人民医院神经内科
基金项目:国家自然科学基金 ( 3994 0 0 12 ),美国CMB基金 ( 0 0 -730 ),教育部归国人员启动基金 ( 199936 3),广东省自然科学基金( 990 0 6 5),广东省医药卫生科研基金 (B19990 35),广东省博士基金( 984 2 2 5),广东省自然科学基金团队项目 ( 2 0 0 0年 ),广东省
摘    要:目的 :探讨实验性大脑皮层梗塞后同侧纹状体、丘脑及对侧脊髓前角的神经结构可塑性。方法 :采用易卒中型肾血管性高血压大鼠制作右侧大脑中动脉皮层支闭塞模型 ,分别于术后第 1周、2周、3周和 4周 ,取鼠脑行免疫组化检查 ,检测大鼠不同时点纹状体、丘脑腹后外侧核及对侧脊髓前角的微管相关蛋白 2 (MAP 2 )、突触生长素(SYN)和生长相关蛋白 (GAP 43)表达的变化。结果 :大脑皮层梗塞后第 1周 ,同侧纹状体、丘脑腹后外侧核和对侧脊髓前角GAP 43阳性信号开始增加 ,第 2周达到高峰 ,之后增加幅度逐渐减弱 ;这些部位SYN阳性信号第 1周较对照组高 ,至第 2周恢复正常 ,第 3周和第 4周逐渐降低 ,且显著低于对照组 ;脑皮层梗塞后第 2周 ,同侧纹状体和丘脑腹后外侧核MAP 2阳性细胞数开始减少 ,至 3周、4周显著低于对照组。结论 :大脑皮层梗死后早期远离梗塞灶的相关神经组织有明显的可塑性 ,后期神经细胞继发性死亡且可塑减缓

关 键 词:脑梗死  易卒中型肾血管性高血压大鼠  神经可塑性
修稿时间:2002-02-20

Neural plasticity of related sites in central nervous system after experimental cerebral cortex infarction in rats
ZENG Jinsheng,LI Hua,FAN Yuhua,et al.. Neural plasticity of related sites in central nervous system after experimental cerebral cortex infarction in rats[J]. China Journal of Rehabilitation Medicine, 2002, 17(2): 69-71
Authors:ZENG Jinsheng  LI Hua  FAN Yuhua  et al.
Affiliation:ZENG Jinsheng,LI Hua,FAN Yuhua,et al.Dept. of Neurology and Stroke Center,First Affiliated Hospital,Sun Yat Sen University,Guangzhou,510080
Abstract:Objective:To observe the neural structural plasticity occurred in ipsilateral striatum, thalamus and contralateral anterior horn of spinal cord after experimental cerebral cortex infarction in rats. Method:At the end of 1st, 2nd, 3rd and 4th week after distal ligation of right middle cerebral artery in renovascular hypertensive rats, the brains and spinal cords were used for immunocytochemical analysis in order to determine the expression of microtubule associate protein 2 (MAP 2), synaptophysin(SYN) and growth associated protein 43(GAP 43) in ipsilateral striatum, thalamus and contralateral anterior horn of spinal cord. Result:GAP 43 positive signal values started to increase at ipsilateral striatum, thalamus and contralateral anterior horn of spinal cord at end of 1st week, reached the peak value at end of 2nd week, then gradually reduced at the end of 3rd and 4th week. SYN positive signal values were higher at ipsilateral striatum, thalamus and contrateral anterior horn of spinal cord at the end of 1st week, then returned to normal level at 2nd week, and reduced to lower level than controls at week 3 and week 4. MAP 2 positive cells reduced at ipsilateral striatum and thalamus at the end of 2nd week, then gradually decreased in 3rd and 4th week. Conclusion:Obvious neural plasticity happens at the related sites in central nervous system after experimental cerebral motorsensory cortex infarction at early stage, but is retarded with secondary neural cells death in the late stage.
Keywords:cerebral infarction  stroke prone renovascular hypertensive rats  neural plasticity
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