Snyder S H, D'Amato R J
Neurology. 1986 Feb;36(2):250-8. doi: 10.1212/wnl.36.2.250.
MPTP (N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) elicits selective destruction of nigrostriatal dopamine neurons in humans and animals along with clinical symptoms of parkinsonism. Recent studies clarify mechanisms accounting for this neurotoxicity. MPTP binds with high affinity to monoamine oxidase, which transforms it to the pyridinium MPP+ . MPP+ is selectively concentrated by the dopamine neuronal uptake system. In nigral cells, binding by melanin of MPP+ affords a "depot" release mechanism to maintain prolonged high intracellular concentrations sufficient to destroy cells. PC-12 cells provide a model catecholamine cell culture for screening environmentally occurring substances that may be relevant in the etiology of idiopathic Parkinson's disease.
MPTP（N-甲基-4-苯基-1,2,3,6-四氢吡啶）会导致人类和动物黑质纹状体多巴胺神经元的选择性破坏，并伴有帕金森氏症的临床症状。最近的研究阐明了这种神经毒性的机制。MPTP与单胺氧化酶具有高亲和力结合，单胺氧化酶将其转化为吡啶鎓MPP⁺。MPP⁺通过多巴胺神经元摄取系统被选择性浓缩。在黑质细胞中，MPP⁺与黑色素的结合提供了一种“储存库”释放机制，以维持足够长时间的高细胞内浓度来破坏细胞。PC-12细胞提供了一种模型儿茶酚胺细胞培养物，用于筛选可能与特发性帕金森病病因相关的环境中存在的物质。
