LOSS OF THE NEURAL INTEGRATOR OF THE OCULOMOTOR SYSTEM FROM BRAIN-STEM LESIONS IN MONKEY
LOSS OF THE NEURAL INTEGRATOR OF THE OCULOMOTOR SYSTEM FROM BRAIN-STEM LESIONS IN MONKEY
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DOI：
10.1152/jn.1987.57.5.1383
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发表时间：
1987-05-01
影响因子：
2.5
通讯作者：
ROBINSON, DA
中科院分区：
文献类型：
--
作者：
CANNON, SC;ROBINSON, DA
在前庭内侧和舌下前位核区域注射神经毒素（kainate或ibotenate）前后，记录了四只幼年恒河猴（Macaca mulatta）的眼球运动，该区域被假设为水平眼球运动命令的神经整合器所在区域。用磁场/眼圈法测量头部受限动物的眼球运动。猴子被训练去跟随视觉目标。在颅骨的环钻孔上植入一个腔室，可以用金属微电极在脑干中进行录音。定位外展神经核，作为后续通过套管注射神经毒素的参考点。这些病变对固定、前庭和光动力学反应以及平滑追踪的影响与由神经整合器缺失引起的预测眼动异常进行了比较。Kainate和ibotenate不会在脑干的这一区域造成永久性损伤。所有的眼球运动在几天到两周的时间内恢复正常。组织学检查显示，导管尖端主要位于前庭和前位舌下核之间，在其吻侧2 mm内，与外展核接壤。密集的胶质瘤清晰地划分了插管轨道，但大多数注射剂周围没有神经元丢失区域。因此，眼动障碍是由于可逆的，而不是永久性的病变。神经积分器的时间常数是在完全黑暗的情况下，根据眼球偏心扫视后的向心漂移速度确定的。对于完整的动物，这个时间常数大于20 s。双侧注射神经毒素后不久，时间常数开始下降，最小可达200 ms；每一次水平扫视之后都有一次快速的向心漂移，时间常数约为200毫秒。对于垂直眼动，在这个急性期，时间常数约为2.5 s。病变使前庭反射（VOR）发生明显改变。在完全黑暗中，头部速度恒定的步幅引起的是眼睛位置的步幅变化，而不是速度的变化。在缺乏神经积分器的情况下，来自椎管传入的阶跃速度指令没有被整合以产生眼位的斜坡（正常的慢相）；相反，这个信号被直接传递给运动神经元，导致眼睛的位置发生变化。头部速度信号的旋转前后衰减时间缩短至5 ~ 6 s，表明前庭速度存储也受到损害。（摘要删节为400字）
Eye movement were recorded from four juvenile rhesus monkeys (Macaca mulatta) before and after the injection of neurotoxins (kainate or ibotenate) in the region of the medial vestibular and prepositus hypoglossi nuclei, an area hypothesized to be the locus of the neural integrator for horizontal eye movement commands. Eye movements were measured in the head-restrained animal by the magnetic field/eye-coil method. The monkeys were trained to follow visual targets. A chamber implanted over a trephine hole in the skull permitted recordings to be made in the brain stem with metal microelectrodes. The abducens nuclei were located and used as a reference point for subsequent neurotoxin injections through cannulas. The effects of these lesions on fixation, vestibuloocular and optokinetic responses, and smooth pursuit were compared with predicted oculomotor anomalies caused by a loss of the neural integrator. Kainate and ibotenate did not create permanent lesions in this region of the brain stem. All the eye movements returned toward normal over the course of a few days to 2 wk. Histological examination revealed that the cannula tips were mainly located between the vestibular and prepositus hypoglossi nuclei, in their rostral 2 mm, bordered rostrally by the abducens nuclei. Dense gliosis clearly demarcated the cannula tracks, but for most injections there were no surrounding regions of neuronal loss. Thus the eye movement disorders were due to a reversible, not a permanent, lesion. The time constant for the neural integrator was determined from the velocity of the centripetal drift of the eyes just after an eccentric saccade in total darkness. For intact animals this time constant was greater than 20 s. Shortly after bilateral injections of neurotoxin, the time constant began to decrease and reached a minimum of 200 ms; every horizontal saccade was followed by a rapid centripetal drift with a time constant of approximately 200 ms. For vertical eye movements, in this acute phase, the time constant was approximately 2.5 s. The vestibuloocular reflex (VOR) was drastically changed by the lesions. A step of constant head velocity in total darkness evoked a step change in eye position rather than in velocity. In the absence of the neural integrator, the step velocity command from the canal afferents was not integrated to produce a ramp of eye position (normal slow phases); rather this signal was relayed directly to the motoneurons and caused a step in eye position. The per- and postrotatory decay of the head velocity signal was decreased to 5-6 s indicating that vestibular velocity storage was also impaired.(ABSTRACT TRUNCATED AT 400 WORDS)