Schultz W, Romo R, Scarnati E, Sundström E, Jonsson G, Studer A
Institute of Physiology, University of Fribourg, Switzerland.
Exp Brain Res. 1989;78(2):253-67. doi: 10.1007/BF00228897.
The oculomotor performance of monkeys was investigated before and after destruction of nigrostriatal dopamine neurons by MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine). Stimulus-triggered saccades and their relationships to arm movements were measured in a reaction time task. Spontaneous eye movements were recorded while monkeys sat in a primate chair and looked around the laboratory without performing any task. In the reaction time task, saccades and arm movements were commonly triggered by the rapid, visible and audible opening of a small food-containing box which was located at a constant position in front of the animal at eye level. Median saccadic latencies ranged from 68 to 118 ms in intact animals. Saccades were followed by onset of electromyographic (EMG) activity in the extensor digitorum communis and the biceps brachii, the prime mover muscles for the following arm reaching movement. Latencies of stimulus-triggered saccades showed an absence of linear relationship to EMG or arm movement reaction time in intact animals (correlation coefficients of 0.15-0.56). This suggests that eye and arm movements were initiated independently from each other in this experimental situation. Treatment with MPTP resulted in 98-99.5% loss of striatal dopamine in both monkeys. This induced a 29-93% increase in saccadic latency in the reaction time task. The sequential occurrence of saccade, EMG activity and arm movement in each trial was preserved, although intervals between onset of saccades and onsets of EMGs and arm movements were prolonged by 53-173% and 33-679% respectively. Onsets of individual saccades remained uncorrelated with onsets of EMG activity or arm movement. Spontaneous eye movements were strongly reduced in frequency and amplitude after MPTP. Administration of the dopamine precursor L-Dopa increased spontaneous eye movements for less than two hours. The severe deficits in stimulus-triggered and spontaneous saccadic eye movements are oculomotor components of hypokinesia arising after MPTP-induced lesions of the nigrostriatal dopamine system in primates. The data are further evidence for a role of midbrain dopamine neurons in behavioral responsiveness and spontaneous activity.
在通过MPTP（1-甲基-4-苯基-1,2,3,6-四氢吡啶）破坏黑质纹状体多巴胺神经元之前和之后，对猴子的动眼神经功能进行了研究。在一项反应时间任务中，测量了刺激触发的扫视及其与手臂运动的关系。当猴子坐在灵长类动物椅子上环顾实验室且不执行任何任务时，记录其自发眼动。在反应时间任务中，扫视和手臂运动通常由位于动物眼前水平固定位置的一个装有食物的小盒子快速、可见且可听到的打开所触发。在完整动物中，中位扫视潜伏期为68至118毫秒。扫视之后是指总伸肌和肱二头肌的肌电图（EMG）活动开始，这两块肌肉是随后手臂伸展运动的主要动力肌。在完整动物中，刺激触发的扫视潜伏期与EMG或手臂运动反应时间不存在线性关系（相关系数为0.15 - 0.56）。这表明在这种实验情况下，眼动和手臂运动是相互独立启动的。用MPTP处理导致两只猴子纹状体多巴胺损失98 - 99.5%。这在反应时间任务中使扫视潜伏期增加了29 - 93%。每个试验中扫视、EMG活动和手臂运动的顺序出现得以保留，尽管扫视开始与EMG和手臂运动开始之间的间隔分别延长了53 - 173%和33 - 679%。单个扫视的开始与EMG活动或手臂运动的开始仍不相关。MPTP处理后，自发眼动的频率和幅度大幅降低。给予多巴胺前体L-多巴可使自发眼动增加不到两小时。刺激触发和自发扫视眼动的严重缺陷是灵长类动物中MPTP诱导的黑质纹状体多巴胺系统损伤后出现的运动减少的动眼神经组成部分。这些数据进一步证明了中脑多巴胺神经元在行为反应性和自发活动中的作用。
