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首页> 外文OA文献 >Differential vulnerability of primate caudate-putamen and striosome-matrix dopamine systems to the neurotoxic effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine
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Differential vulnerability of primate caudate-putamen and striosome-matrix dopamine systems to the neurotoxic effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine

机译：灵长类尾状-酪氨酸和基质体-多巴胺系统对1-甲基-4-苯基-1,2,3,6-四氢吡啶的神经毒性作用的差异脆弱性

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The meperidine analogue derivative 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induces nigrostriatal fiber damage and severe parkinsonism in humans and animals. MPTP-induced parkinsonism has been proposed as a model of Parkinson disease, but doubts have been raised about whether the patterns of nigrostriatal fiber loss in the two conditions are similar. We report here observations on [3H]mazindol monoamine (principally dopamine) uptake-site binding in the striatum of monkeys (Saimiri sciureus) exposed to low doses of MPTP. We show that this treatment can produce a pattern of nigrostriatal degeneration characteristic of that seen in Parkinson disease, in which there is greater depletion of dopaminergic markers in the putamen than in the caudate nucleus, especially posteriorly. Moreover, within the regions of diminished uptake-site binding in the MPTP-treated monkeys, there is differential preservation of binding in striosomes relative to the surrounding matrix. We suggest that both regional and striosome/matrix patterns of nigrostriatal depletion are key features of MPTP-induced neurodegeneration and that both patterns may provide clues to the mechanisms underlying neurodegeneration in Parkinson disease as well
机译：哌替啶类似物衍生物1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）在人类和动物中诱发黑纹状体纤维损伤和严重的帕金森氏病。已经提出了MPTP诱导的帕金森病作为帕金森氏病的模型，但是人们怀疑在两种情况下黑质纹状体纤维丢失的模式是否相似。我们在此报告对低剂量MPTP暴露的猴子（Saimiri sciureus）纹状体中[3H] mazindol单胺（主要是多巴胺）摄取位点的观察结果。我们显示这种治疗可以产生一种在帕金森病中所见的黑质纹状体变性特征，其中在壳状核中比在尾状核中，特别是在后核中，多巴胺能标记的消耗更大。此外，在经MPTP处理的猴子中，摄取位点结合减少的区域内，相对于周围基质，在脂质体中结合的保持差异。我们建议，黑质纹状体耗竭的区域和纹状体/基质模式都是MPTP诱导的神经退行性变的关键特征，并且这两种模式都可能为帕金森病神经退行性变的潜在机制提供线索

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