帕金森小鼠多巴胺能神经元轴突超微结构研究

目的研究1-甲基4苯基-1，2，3，6-四氢吡啶（MPTP）诱导的小鼠多巴胺能神经元轴突变性的超微结构改变，探讨其在帕金森病发病机制中的作用。方法应用免疫组织化学染色、电镜分析等方法，观察MPTP诱导的小鼠黑质-纹状体多巴胺能神经元轴突变性与神经元损伤的超微结构变化，探讨神经元损伤与细胞轴突损伤的相互关系。结果MPTP可诱导小鼠产生典型的帕金森病症状，并可引起黑质-纹状体多巴胺能神经元的凋亡与轴突变性。但在超微结构变化上存在时间差异性，轴突微管的损伤发生较早，而典型的神经元凋亡改变出现较晚。结论轴突变性在帕金森病发病机制中起着十分重要的作用。可能独立于其胞体的凋亡，甚至可能是神经元凋亡的诱因，因此阻止轴突变性，有可能为帕金森病的治疗提供新的策略。

The study of axonul ultrastructure of dopaminergic neurons in mice models of Parkinson's disease

Objective To study the axonal uhrastructure of dopaminergic neurons in Parkinson＇s disease （PD） mice models and to explore the crucial role of axonal degeneration in the pathogenesis of Parkinson＇s disease. Methods Immunohistochemistry staining and transmission electron microscope were used to observe the uhrastructural changes of nigra neurons death and axonal degeneration induced by MPTP. The relationship between apoptosis and axonal degeneration was analyzed. Results MPTP could induce typical Parkinsonism in mice, neuronal apoptosis and axonal degeneration of dopaminergic neurons. But there was significant temporal difference in the ultrastructural alteration. The axonal degeneration appeared earlier than neurons apoptosis. Conclusion Axonal degeneration plays a crucial role in the pathogenesis of the PD. It may be independent of neurons apoptosis and even be the inducement of neuronal apoptosis. Preventing axonal degeneration may be a new therapeutic strategy to Parkinson＇s disease.