EFFECTS OF N-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE AND ITS METABOLITE, N-METHYL-4-PHENYLPYRIDINIUM ION, ON DOPAMINERGIC NIGROSTRIATAL NEURONS IN THE MOUSE
EFFECTS OF N-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE AND ITS METABOLITE, N-METHYL-4-PHENYLPYRIDINIUM ION, ON DOPAMINERGIC NIGROSTRIATAL NEURONS IN THE MOUSE
复制标题
DOI：
10.1016/0304-3940(85)90074-6
复制
发表时间：
1985-01-01
影响因子：
2.5
通讯作者：
WRIGHT, JM
中科院分区：
文献类型：
--
作者：
PERRY, TL;YONG, VW;WRIGHT, JM
C57 黑小鼠单次皮下注射 40 mg/kg N-甲基-4-苯基-1,2,3,6-四氢吡啶 (MPTP) 会导致纹状体多巴胺消耗 90%，并导致黑质致密带神经元细胞体损失 33%。到 4.5 个月时，纹状体多巴胺能功能似乎部分恢复。注射到小鼠体内后，MPTP 代谢物 N-甲基-4-苯基吡啶鎓离子 (MPP+) 进入纹状体，并通过某种未知机制比 MPTP 毒性更大。然而，重复注射最大耐受量的 MPP+ 不会损害多巴胺能黑质纹状体神经元。
A single subcutaneous injection in the C57 black mouse of 40 mg/kg of N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes a 90% depletion of striatal dopamine, as well as loss of 33% of neuronal cell bodies in the substantia nigra, zona compacta. By 4.5 months, there appears to be partial recovery of striatal dopaminergic function. After injection into mice, the MPTP metabolite, N-methyl-4-phenylpyridinium ion (MPP+) enters the striatum, and through some unknown mechanism is even more toxic than MPTP. However, repeated injections of maximally tolerated amounts of MPP+ do not damage dopaminergic nigrostriatal neurons.