CEREBELLAR-DEPENDENT ADAPTIVE-CONTROL OF PRIMATE SACCADIC SYSTEM
CEREBELLAR-DEPENDENT ADAPTIVE-CONTROL OF PRIMATE SACCADIC SYSTEM
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DOI：
10.1152/jn.1980.44.6.1058
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发表时间：
1980-01-01
影响因子：
2.5
通讯作者：
ROBINSON, DA
中科院分区：
文献类型：
--
作者：
OPTICAN, LM;ROBINSON, DA
在恒河猴身上证明了中枢神经系统补偿跳动困难的能力。对小脑消融后这种适应机制的行为进行了检测。猴子被训练成注视小目标光。当动物坐在旋转的磁场中，头部固定时，眼睛的运动被监测。1眼肌腱切除后水平直肌肌力减弱。这只虚弱的眼睛产生的眼跳是低速的，随后是眼跳后的漂移。当切换眼罩以使弱眼观看时，弱眼产生的高度眼跳逐渐变得更大。3天后，他们基本上是矫形的。中枢神经系统显然弥补了外周的弱点。肌腱切除手术降低了肌肉的力量，产生了子宫下层，扰乱了眼眶内粘性与弹性的比例，导致弱眼的眼球后跳动。进行扫视所需的神经有阶段性和紧张性成分，即所谓的脉搏和台阶。眼跳修复机制增加脉搏和阶梯以补偿子宫下层，并调整脉搏和阶梯的比例以消除眼球后漂移。对2只猕猴进行了小脑全切除手术，每只猴1只眼去腱。这些消融在两种动物未手术的眼睛中造成并持续着跳动过大和跳动后的漂移。全小脑切除取消了所有眼球跳动系统的适应性修复。对2只猕猴行小脑部分切除术，每只猴1只眼去腱。在两种动物未手术的眼球中，蚯蚓和副眼(叶IV-IX)和顶核的损伤造成了持续性的跳动过多，而没有跳动后的漂移。这些病变取消了对神经脉冲的适应性控制。神经支配步骤中的适应性变化仍然发生，因此在有经验的观察眼中，眼球后漂移总是被消除。小脑中线(蚯蚓、穹隆旁和顶核)似乎对眼球运动障碍的修复很重要，但对眼球后漂移的修复并不重要。脉络膜切除术后视网膜滑脱不能得到补偿。步长的自适应控制可能依赖于小叶。在小脑受损后，猴子能够做出所有幅度和方向的眼跳。这些动物的主要缺陷似乎是神经的脉冲和步骤不再适合目标移位。S的小脑对眼球跳动的主要贡献是调节脉搏和台阶产生机制的增益。显然，心律失常的修复是小脑的普遍功能。
The ability of the CNS to compensate for saccadic dysmetria was demonstrated in rhesus monkeys. The behavior of this adaptive mechanism after cerebellar ablations was examined. Monkeys were trained to fixate small target lights. Eye movements were monitored while the animals were seated with their heads fixed, in a rotating magnetic field. The horizontal recti muscles of 1 eye were weakened by tenectomy. Saccades made by this weakened eye were hypometric, and followed by postsaccadic drift. When the patch was switched so that the weak eye was viewing, the hypometric saccades made by the weak eye gradually became larger. After 3 days they were essentially orthometric. The CNS apparently compensated for a peripheral weakness. The tenectomy operation reduced the strength of the muscles, creating hypometria, and upset the ratio of viscosity to elasticity in the orbit, producing postsaccadic drift in the weak eye. The innervation required to make a saccade has phasic and tonic components, the so-call pulse and step. The saccadic repair mechanism increased the pulse and the step to compensate for the hypometria, and adjusted the ratio of the pulse to the step to eliminate postsaccadic drift. Total cerebellectomies were performed on 2 monkeys with 1 tenectomized eye each. These ablations created and enduring saccadic hypermetria and postsaccadic drift in the unoperated eye of both animals. The total cerebellectomy abolished all adaptive repair of the saccadic system. Partial cerebellectomies were performed on 2 monkeys, each of which had 1 tenectomized eye. Lesions of the vermis and paravermis (lobes IV-IX) and the fastigial nuclei created an enduring saccadic hypermetria, without postsaccadic drift in the unoperated eye of both animals. The lesions abolished adaptive control of the pulse of innervation. Adaptive changes in the step of innervation still occurred, so that postsaccadic drift was always eliminated in the experienced, viewing eye. The midline cerebellum (vermis, paravermis and fastigial nuclei) appears important for repair of saccadic dysmetria, but not for repair of postsaccadic drift. Postsaccadic retinal slip was not compensated for in flocculectomized monkeys. The adaptive control of the step may depend on the flocculus. After cerebellar lesions the monkeys were able to make saccades of all amplitudes and directions. The principal deficit in these animals seemed to be that the pulse and step of innervation were no longer appropriate to the target displacement. The cerebellum''s principal contribution to saccadic eye movements is the adjustment of the gains of the pulse- and step-generating mechanisms. Repair of dysmetria apparently is a general function of the cerebellum.