Chen S
Department of Neurology, Ren Ji Hospital, Shanghai Second Medical University.
Zhonghua Shen Jing Jing Shen Ke Za Zhi. 1992 Feb;25(1):50-2, 64.
Infusion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) into the right common carotid artery of 5 rhesus monkeys produced hemiparkinsonian syndrome in the contralateral limbs which responded to madopa or apomorphine therapy. Moreover, these two drugs induced circling away from the MPTP-treated side, amphetamine induced rotation toward the MPTP-treated side. Long-term use of madopa developed a peak-dose dyskinesia of the face and the limbs contralateral to the MPTP-treated side. The ipsilateral toxic effects were confirmed biochemically by reduction of nigrostriatal DA and histologically by degeneration of nigral neurons of the MPTP-treated side. It is concluded that this hemiparkinsonian model of rhesus monkey will be of value in the elucidation of the neural mechanism underlying L-DOPA or DA agonist induced dyskinesia in Parkinson's disease and in the search for newer methods of treatment which would produce less dyskinesia and response fluctuations.
向5只恒河猴的右侧颈总动脉注射1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP),在对侧肢体产生偏侧帕金森综合征,该综合征对美多巴或阿扑吗啡治疗有反应。此外,这两种药物会诱导动物向远离MPTP治疗侧的方向转圈,而苯丙胺会诱导动物向MPTP治疗侧旋转。长期使用美多巴会在MPTP治疗侧对侧的面部和肢体出现峰值剂量运动障碍。通过黑质纹状体多巴胺减少在生化方面证实了同侧毒性作用,通过MPTP治疗侧黑质神经元变性在组织学方面证实了同侧毒性作用。结论是,这种恒河猴偏侧帕金森模型对于阐明帕金森病中左旋多巴或多巴胺激动剂诱导的运动障碍的神经机制以及寻找能产生较少运动障碍和反应波动的新治疗方法具有价值。