偏侧帕金森病猴模型黑质和纹状体一氧化氮合酶表达的变化

目的探讨偏侧帕金森病（PD）猴模型黑质和纹状体一氧化氮合酶（NOS）表达的变化。方法对3只恒河猴经单侧颈内动脉注射1-甲基4-苯基1，2，3，6-四氢吡啶（MPTP）制备成偏侧PD猴模型后，应用还原型尼克酰胺腺嘌呤二核苷酸-黄递酶（NADPH．d）组化染色方法观察偏侧PD猴黑质和纹状体NOS阳性神经元表达的变化，并与正常猴比较。结果偏侧PD猴MPTP毁损侧的黑质和纹状体的NOS阳性神经元数目较毁损对侧和正常猴明显增加（均P〈0．01），毁损对侧的黑质和纹状体NOS阳性神经元数目与正常猴比较差异无统计学意义。结论偏侧PD猴黑质和纹状体NOS阳性神经元增多，由此引起一氧化氮（NO）合成和释放增多，可能对黑质和纹状体神经元的变性和死亡起重要作用。

Expressing changes of nitric oxide synthase in substantia nigra and striatum of hemiparkinsonism monkey model

Objective To investigate the expressing changes of nitric oxide synthase(NOS) in substantia nigra and striatum of the hemiparkinsonism monkey model.Methods Three hemiparkinsonian rhesus monkey models were induced by injecting 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP) unilaterally into the internal carotid artery.The expressing changes of NOS-positive neurons of substantia nigra and striatum in three hemiparkinsonism monkey models and one normal control monkey were observed by using NADPH-diaphorase histochemistry staining method.Results The NOS-positive neurons were increased significantly in the substantia nigra and striatum of MPTP lesioned side of hemiparkinsonian monkey model compared to contralateral side and normal control monkey(all P<0.01),and no difference was found between contralateral side and normal control monkey.Conclusion The excessive production of NO secondary to the increment of NOS-positive neurons in the substantia nigra and striatum of hemiparkinsonian monkey models can play important role in the mechanism of neuronal degeneration and death.