大鼠局灶性脑缺血-再灌注后尾壳核神经型一氧化氮合酶表达的变化

目的：探讨神经型一氧化氮合酶（Neuronal nitric oxide synthase,nNOS)在大鼠脑缺血后不同时程尾壳核内的变化。方法：应用大鼠大脑中动脉阻塞模型（MCAO）,结合免疫细胞化学ABC法和图像定量分析技术进行研究。结果：缺血－再灌注早期（0h,1h,6h)尾壳核内nNOS免疫反应阳性神经元数量减少,细胞形态变圆,树突缩短,形态学参数开始下降,缺血－再灌注中期（24h,48h,72h)nNOS阳性神经元数量和形态学参数较前有一过性升高,但随后仍持续降低,缺血－再灌注后期（1W）nNOS阳性神经元数量继续下降,胞体浓缩,树突消失,细胞崩解,形态学参数降到最低,结论：脑缺血－再灌注后尾壳核内nNOS免疫反应阳性神经元损伤较重,持续时间长,后期更为严重,这可能会影响尾壳核功能的恢复。

CHANGES OF NEURONAL NITRIC OXIDE SYNTHASE EXPRESSION IN RAT CAUDATE-PUTAMEN NUCLEUS AFTER LOCAL CEREBRAL ISCHEMIA

Objective:To investigate the changes of neuronal nitric oxide synthase (nNOS) expression in caudate putamen nucleus after cerebral ischemia.Methods:The model of middle cerebral artery occlusion (MCAO) was used,the methods of immunocytochemical and morphometric quantitative analysis system was employed to study the changes in different stage after brain ischemia refusion.Results:At early stage after brain ischemia refusion (0 h,1 h,6 h),the number and morphological parameters of nNOS immunopositive neurons declined,the cell body became round,and the dendrite became short;At the middle stage of ischemia refusion (24 h,48 h,72 h),The number and morphology parameter of nNOS immunopositive neurons had a transient rise,then it declined continuously;At the later period (1 W),the number of nNOS immunopositive neurons persistently reduced,the body of neuron concentrated or disintegrated,the dendrite disappeared.Conclusion:The brain ischemia refusion has severe damage on the nNOS positive neuron in caudate putamen nucleus,and it may affect the function of caudate putamen nucleus and the message transmission of extrapyramidal system restoration.