Donnan G A, Willis G L, Kaczmarczyk S J, Rowe P
J Neurol Sci. 1987 Feb;77(2-3):185-91. doi: 10.1016/0022-510x(87)90121-3.
Motor function was assessed by use of a swim test in C57 Black mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Thirty minutes after the last MPTP injection significant motor impairment was observed while striatal dopamine was reduced to 13.9% of control levels. At 24 h and 7 days post MPTP injection dopamine levels were still reduced to 17.3% and 26.4% of control values but swimming abilities of the mice were unimpaired. Histofluorescence of catecholaminergic neurons confirmed the presence of catecholamine depletion but showed little evidence of neuronal destruction. The use of MPTP as a non-invasive means of nigrostriatal dopamine depletion in rodents and higher animals allows a re-evaluation of the role of the dopaminergic system in the modulation of movement.
通过在接受1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）治疗的C57黑小鼠中进行游泳测试来评估运动功能。在最后一次注射MPTP后30分钟，观察到明显的运动障碍，而纹状体多巴胺减少至对照水平的13.9%。在注射MPTP后24小时和7天，多巴胺水平仍分别降至对照值的17.3%和26.4%，但小鼠的游泳能力未受损。儿茶酚胺能神经元的组织荧光证实了儿茶酚胺耗竭的存在，但几乎没有神经元破坏的证据。使用MPTP作为啮齿动物和高等动物黑质纹状体多巴胺耗竭的非侵入性手段，可以重新评估多巴胺能系统在运动调节中的作用。
