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首页> 外文期刊>The European Journal of Neuroscience >Persistent penetration of MPTP through the nasal route induces Parkinson's disease in mice.
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Persistent penetration of MPTP through the nasal route induces Parkinson's disease in mice.

机译：MPTP持续通过鼻途径渗透会诱发小鼠帕金森氏病。

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摘要

The aetiology of idiopathic Parkinson's disease (PD) is poorly defined but environmental aggression may be relevant. Here, we report a new model of PD in mice, based on chronic inoculation with neurotoxins in the nasal cavity, which is a natural route of contact with the environment. C57BL/6 mice, submitted to daily intranasal inoculation with MPTP for 30 days, developed motor deficits that correlated with a progressive and severe depletion of striatal dopamine levels, and loss of tyrosine hydroxylase and dopamine transporter staining in substantia nigra and striatum. Moreover, mice intranasally inoculated with MPTP developed strong astrogliosis and microgliosis in substantia nigra and striatum. Consistent with these observations, a role for oxidant aggression was demonstrated by increased levels of Mn-superoxide dismutase. However, alpha-synuclein aggregation was not observed. This new animal model provides a new tool for studying PD symptoms that develop slowly over time, and it may be used to asses risk from environmental neurotoxins.
机译：特发性帕金森病（PD）的病因学定义不清，但环境侵略性可能与此有关。在这里，我们报告了一种新型的PD小鼠模型，其基于在鼻腔中长期接种神经毒素，这是与环境接触的自然途径。每天接受MPTP鼻内接种30天的C57BL / 6小鼠出现运动缺陷，其与纹状体多巴胺水平的进行性和严重消耗，黑质和纹状体中酪氨酸羟化酶和多巴胺转运蛋白染色的丧失有关。此外，鼻内接种MPTP的小鼠在黑质和纹状体中出现了强烈的星形胶质细胞变性和小胶质细胞变性。与这些观察结果一致，锰超氧化物歧化酶水平的增加证明了氧化剂的侵害作用。但是，未观察到α-突触核蛋白聚集。这种新的动物模型为研究随时间缓慢发展的PD症状提供了一种新工具，并且可以用于评估环境神经毒素的风险。

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