Kopin I J, Markey S P
National Institute of Neurological and Communicative Disorders and Stroke, Bethesda, Maryland 20892.
Annu Rev Neurosci. 1988;11:81-96. doi: 10.1146/annurev.ne.11.030188.000501.
In summary, the parkinsonism induced by MPTP in man closely resembles time-telescoped Parkinson's disease. Parkinsonian symptoms can be duplicated in all aspects under controlled conditions in subhuman primates; the biochemical changes are replicated in mice, dogs, and to varying degrees in other species. Mechanisms of bioactivation by MAO-B of MPTP to MPP+, concentration of MPP+ in neurons with a catecholamine uptake system, and vulnerability to cellular toxic effects of MPP+ are the basis for the specificity of MPTP targeting of nigrostriatal dopaminergic neurons. It is hoped that an understanding of the mechanism of species specificity and cellular toxicity will in time explain the pathogenesis of idiopathic Parkinson's disease and suggest new opportunities for effective therapy.
总之,MPTP在人体诱发的帕金森综合征与时间压缩型帕金森病极为相似。在可控条件下,帕金森症状在非人灵长类动物身上各方面均可重现;生化变化在小鼠、狗及其他物种身上也有不同程度的复制。MAO-B将MPTP生物激活为MPP+的机制、具有儿茶酚胺摄取系统的神经元中MPP+的浓度以及对MPP+细胞毒性作用的易感性,是MPTP靶向黑质纹状体多巴胺能神经元特异性的基础。希望对物种特异性和细胞毒性机制的理解,能及时解释特发性帕金森病的发病机制,并为有效治疗提供新的契机。