[帕金森病的实验模型:MPTP神经毒性的机制和解剖病理特征]。

Archivos de neurobiologia Pub Date : 1992-07-01
M T Herrero, M R Luquín, J A Obeso
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引用次数: 0

摘要

在动物和人类中,MPTP给药诱导了相当选择性的黑质多巴胺能神经元损伤。MPTP的这一特点导致了帕金森病和神经元变性的最佳可用模型。MPP+的作用机制可能包括:1)线粒体损伤。2)自由基生成。3)高黑化神经元捕获MPP+。本文就MPTP的毒性作用机制及其神经病理特点作一综述。
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[Experimental model of Parkinson disease: mechanisms and anatomo- pathological characteristics of MPTP neurotoxicity].

MPTP administration induces a fairly selective lesion of substantia nigra dopaminergic neurons both in animals and humans. This characteristic of MPTP has led to the best available model of Parkinson's disease and neuronal degenerations. MPTP toxicity is actually provoked by MPP+ which results after oxidation by MAO-B. Possible mechanism of action of MPP+ include: 1) Mitochondrial lesion. 2) Free radicals generation. 3) Trapping of MPP+ by highly melanized neurons. This article reviews the mechanisms of toxicity by MPTP and its neuropathological characteristics.

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