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首页> 外文期刊>Neuropathology and applied neurobiology >Evidence of oligodendrogliosis in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinsonism
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Evidence of oligodendrogliosis in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinsonism

机译：1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱发的帕金森病中少突胶质细胞增生的证据

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Aims: Mice and nonhuman primates administered with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) represent elective experimental models of Parkinsonism, in which degeneration of the nigrostriatal dopaminergic pathway is associated with prominent neuroinflammation, characterized by activated microglia and astrocytes in both substantia nigra (SN) and striatum. To date, it is unknown whether oligodendrocytes play a role in these events. Methods: We performed a detailed qualitative and quantitative analysis of oligodendrocyte-associated changes induced by acute and chronic MPTP treatment, in the SN and striatum of mice and macaques respectively. Oligodendrocytes were immunolabelled by cell-specific markers and analysed by confocal microscopy. Results: In both experimental models, MPTP treatment induces an increase in oligodendrocyte cell number and average size, as well as in the total area occupied by this cell type per tissue section, accompanied by evident morphological changes. This multifaceted array of changes, herein referred to as oligodendrogliosis, significantly correlates with the reduction in the level of dopaminergic innervation to the striatum. Conclusions: This event, associated with early damage of the dopaminergic neurone axons and of the complex striatal circuits of which they are part, may result in an important, although neglected, aspect in the onset and progression of Parkinsonism.
机译：目的：给予1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）的小鼠和非人类灵长类动物代表帕金森病的选择性实验模型，其中黑质纹状体多巴胺能途径的变性与明显的神经炎症相关，其特征是是由黑质（SN）和纹状体中的激活的小胶质细胞和星形胶质细胞引起的。迄今为止，还不知道少突胶质细胞是否在这些事件中起作用。方法：我们对小鼠和猕猴的SN和纹状体分别进行了急性和慢性MPTP处理诱导的少突胶质细胞相关变化的详细定性和定量分析。少突胶质细胞通过细胞特异性标记物进行免疫标记，并通过共聚焦显微镜进行分析。结果：在两个实验模型中，MPTP处理均会导致少突胶质细胞数量和平均大小以及该细胞类型在每个组织切片中占据的总面积增加，并伴有明显的形态变化。这种变化的多方面变化，在本文中称为少突胶质细胞增生，与多巴胺能对纹状体的神经支配水平的降低显着相关。结论：该事件与多巴胺能神经元轴突及其所参与的复杂纹状体回路的早期损害有关，可能导致帕金森氏病发作和发展的一个重要方面，尽管被忽略了。

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