Schneider J S, Unguez G, Yuwiler A, Berg S C, Markham C H
Department of Neurology, Hahnemann University School of Medicine, Philadelphia, PA 19102.
Brain. 1988 Dec;111 ( Pt 6):1265-85. doi: 10.1093/brain/111.6.1265.
Six adult Macaca fascicularis monkeys were trained to perform an instrumentally conditioned, visually-guided forearm reaching task for fruit juice reinforcement. Once animals were overtrained on this task, they were given intravenous injections of N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (0.15 to 0.33 mg/kg). Animals were tested daily for performance in the previously learned behavioural task and were assessed daily for abnormalities in motor functioning. Monkeys developed deficits in operant task performance characterized by termination of responses after an initial series of responses and long pauses between responses. Once an animal stopped responding to the task, responses could often be reinitiated if the experimenter guided the monkey through the task. This type of performance deficit was seen both before and without the appearance of distinct parkinsonian motor signs. Animals which developed motor signs had extensive ventral mesencephalic cell loss while an animal with performance deficits but without motor signs had cell loss restricted to the ventral substantia nigra pars compacta. The results demonstrate that operant performance deficits can be observed in MPTP-treated monkeys independent of the appearance of motor deficits.
六只成年食蟹猴接受训练，执行一项以果汁强化为目的、由视觉引导的工具性条件反射前臂够物任务。一旦动物在该任务上过度训练，就给它们静脉注射N-甲基-4-苯基-1,2,3,6-四氢吡啶（0.15至0.33毫克/千克）。每天测试动物在先前学会的行为任务中的表现，并每天评估其运动功能异常情况。猴子在操作性任务表现中出现缺陷，其特征是在最初一系列反应后反应终止，且反应之间有长时间停顿。一旦动物停止对任务做出反应，如果实验者引导猴子完成任务，反应通常可以重新开始。这种类型的表现缺陷在明显的帕金森运动体征出现之前和没有出现时都能看到。出现运动体征的动物有广泛的中脑腹侧细胞损失，而有表现缺陷但无运动体征的动物细胞损失仅限于黑质致密部腹侧。结果表明，在MPTP处理的猴子中可以观察到操作性表现缺陷，而与运动缺陷的出现无关。
