Gomez-Mancilla B, Bédard P J
Centre de Recherche en Neurobiologie, Hôpital de l'Enfant-Jésus, Québec, Canada.
Clin Neuropharmacol. 1993 Oct;16(5):418-27. doi: 10.1097/00002826-199310000-00004.
A group of four monkeys was rendered parkinsonian with the toxin MPTP. They were then treated chronically with L-DOPA/benserazide 50/12.5 mg/kg given orally daily for 2 months. This dose produced a striking antiparkinsonian effect, but all animals manifested dyskinesia. A series of agents acting primarily on neurotransmitters other than dopamine were then tested in combination with L-DOPA to see if the dyskinetic movements would be modified. Several drugs, including clonidine, physostigmine, methysergide, 5-MDOT, propranolol, and MK-801, markedly reduced the dyskinetic movements but at the cost of a return of parkinsonian symptomatology. However, yohimbine and meperidine reduced predominantly the dyskinetic movements. Baclofen was also useful in one monkey against a more dystonic form of dyskinesia. Atropine converted the dystonic movements into chorea.
一组四只猴子用毒素MPTP诱导出帕金森病。然后它们长期接受口服左旋多巴/苄丝肼50/12.5毫克/千克的治疗,持续2个月。这个剂量产生了显著的抗帕金森病效果,但所有动物都出现了运动障碍。然后测试了一系列主要作用于多巴胺以外神经递质的药物与左旋多巴联合使用,看是否能改善运动障碍性运动。几种药物,包括可乐定、毒扁豆碱、甲基麦角新碱、5-MDOT、普萘洛尔和MK-801,显著减少了运动障碍性运动,但代价是帕金森病症状复发。然而,育亨宾和哌替啶主要减少了运动障碍性运动。巴氯芬对一只猴子对抗一种更具张力障碍形式的运动障碍也有帮助。阿托品将张力障碍性运动转变为舞蹈症。