Ricaurte G A, Langston J W, Delanney L E, Irwin I, Peroutka S J, Forno L S
Brain Res. 1986 Jun 18;376(1):117-24. doi: 10.1016/0006-8993(86)90905-4.
The effect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on nigrostriatal dopaminergic neurons in the mouse was re-examined in view of recent conflicting reports regarding the neurotoxic effect of MPTP in this experimental animal. It was found that while MPTP destroyed a substantial number of dopaminergic nerve terminals in the striatum of young mature (6-8 weeks old) mice, it left the majority of cells in the pars compacta of the substantia nigra (SNc) unaffected. It was also found that 5 months after MPTP treatment there was substantial, although incomplete, recovery of striatal DA nerve terminal markers (DA level, metabolites, uptake, [3H]mazindol binding). Given these observations, it is concluded that while the young mature MPTP mouse may not be a valid animal model of Parkinson's disease (since it does not develop severe SNc cell loss characteristic of this disorder), it will be valuable for the study of how MPTP destroys dopaminergic nerve terminals and may prove useful as an experimental system for studying recovery of dopaminergic fibers after injury and for exploring ways to accelerate this recovery.
鉴于最近关于1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）对该实验动物的神经毒性作用存在相互矛盾的报道，我们重新研究了MPTP对小鼠黑质纹状体多巴胺能神经元的影响。研究发现，虽然MPTP破坏了年轻成熟（6-8周龄）小鼠纹状体中大量的多巴胺能神经末梢，但黑质致密部（SNc）的大多数细胞未受影响。还发现，MPTP治疗5个月后，纹状体多巴胺能神经末梢标记物（多巴胺水平、代谢产物、摄取、[3H]马吲哚结合）有显著但不完全的恢复。基于这些观察结果，得出结论：虽然年轻成熟的MPTP小鼠可能不是帕金森病的有效动物模型（因为它不会出现该疾病特有的严重SNc细胞损失），但它对于研究MPTP如何破坏多巴胺能神经末梢将具有重要价值，并且可能被证明是研究损伤后多巴胺能纤维恢复以及探索加速这种恢复方法的有用实验系统。
