ROLE OF THE CAUDAL FASTIGIAL NUCLEUS IN SACCADE GENERATION .2. EFFECTS OF MUSCIMOL INACTIVATION
ROLE OF THE CAUDAL FASTIGIAL NUCLEUS IN SACCADE GENERATION .2. EFFECTS OF MUSCIMOL INACTIVATION
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DOI：
10.1152/jn.1993.70.5.1741
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发表时间：
1993-11-01
影响因子：
2.5
通讯作者：
FUCHS, AF
中科院分区：
文献类型：
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作者：
ROBINSON, FR;STRAUBE, A;FUCHS, AF
1. 我们研究了暂时抑制两只恒河猴尾顶核神经元的效果，这些恒河猴经过训练可以向跳跃目标进行眼跳。我们在几分钟前记录到眼跳相关神经元的尾顶核部位单侧或双侧注射了γ-氨基丁酸（GABA）激动剂蝇蕈醇。2．单侧注射 (n = 9) 使注射侧高测量和另一侧低测量产生水平扫视（10 度目标步长的平均增益分别为 1.37 和 0.6 1，20 度目标步长的平均增益分别为 1.26 和 0.81；正常扫视增益为 0.96）。垂直目标的扫视显示出小但明显的远视，并且向注射侧强烈弯曲。所有目标眼跳的轨迹和终点比正常情况变化更大。3．单侧注射后，向心性眼跳略大于离心式眼跳（10度目标步长时同侧眼跳平均增益分别为1.42和1.31，20度目标步长时同侧眼跳平均增益为1.37和1.15）。4．单侧注射增加了同侧眼跳的平均加速度并降低了对侧眼跳的加速度。注射降低了垂直扫视的加速度和减速度。5．在测量失调的扫视之后，猴子通过异常大量的测量不足的校正扫视来获得目标。注射使 10 度水平目标步进后的平均纠正眼跳次数从 0.6 次增加到 2.1 次，在 20 度水平目标步进后从 0.8 次增加到 2.1 次。系列中每个连续纠正性扫视的大小减小，并且前一次纠正性扫视的延迟时间增加。6．双侧注射（n = 2）蝇蕈醇，我们首先注射到左侧尾顶核，然后在 30 分钟内注射到右侧，使所有眼跳过度测量（右、左、上和下眼跳 10 度的平均增益分别为 1. 18、1.49、1.43 和 1.10）。矛盾的是，双侧注射同时降低了眼跳加速度和减速度。眼跳轨迹和终点比正常情况变化更大。7．为了解释注射的影响，我们提出一侧尾顶神经元的活动通常有助于减缓同侧眼跳，并通过影响脑干中眼跳突发发生器的反馈回路来帮助加速对侧眼跳。如果没有尾顶活动，脑干爆发发生器就会产生超测量的、可变的眼跳。因此，我们还提出，尾顶神经元对突发发生器的影响使眼跳更加一致和准确。8．我们的注射引起的动眼神经缺陷与瓦伦堡综合征的症状基本相同。我们认为，损伤位于外侧髓质的瓦伦堡患者的动眼神经缺陷实际上是由尾顶神经元的慢性抑制造成的。当髓质病变中断橄榄小脑纤维时，这种抑制就会发生，橄榄小脑纤维与传入眼跳相关顶神经元的小脑皮层部分结合。
1. We studied the effect of temporarily inhibiting neurons in the caudal fastigial nucleus in two rhesus macaques trained to make saccades to jumping targets. We placed injections of the gamma-aminobutyric acid (GABA) agonist muscimol unilaterally or bilaterally at sites in the caudal fastigial nucleus where we had recorded saccade-related neurons a few minutes earlier.2. Unilateral injections (n = 9) made horizontal saccades to the injected side hypermetric and those to the other side hypometric (mean gain of 1.37 and 0.6 1, respectively, for 10-degrees target steps, and 1.26 and 0.81 for 20-degrees target steps; normal saccade gain was 0.96). Saccades to vertical targets showed a small but significant hypermetria and curved strongly toward the side of the injection. The trajectories and end points of all targeted saccades were more variable than normal.3. After unilateral injections, centripetal saccades were slightly larger than centrifugal saccades (mean gains for ipsilateral saccades were 1.42 and 1.31, respectively, for 10-degrees target steps, and 1.37 and 1.15 for 20-degrees target steps).4. Unilateral injections increased the average acceleration of ipsilateral saccades and decreased the acceleration of contralateral saccades. Injections decreased both the acceleration and deceleration of vertical saccades.5. After dysmetric saccades, monkeys acquired the target with an abnormally high number of hypometric corrective saccades. Injection increased the average number of corrective saccades from 0.6 to 2.1 after 10-degrees horizontal target steps and from 0.8 to 2.1 after 20-degrees steps. The size of each successive corrective saccade in a series decreased, and the latency from the previous corrective saccade increased.6. Bilateral injections (n = 2) of muscimol, in which we injected first into the left caudal fastigial nucleus and then, within 30 min, into the right, made all saccades hypermetric (mean gain for 10-degrees right, left, up, and down saccades was 1. 18, 1.49, 1.43, and 1.10, respectively). Paradoxically, bilateral injection decreased both saccade acceleration and deceleration. Saccade trajectories and end points were more variable than normal.7. To account for the effects of our injections, we propose that the activity of caudal fastigial neurons on one side normally helps to decelerate ipsilateral saccades and helps to accelerate contralateral saccades by influencing the feedback loop of the saccade burst generator in the brain stem. Without caudal fastigial activity the brain stem burst generator produces hypermetric, variable saccades. We therefore also propose that the influence of caudal fastigial neurons on the burst generator makes saccades more consistent and accurate.8. Our injections caused oculomotor deficits that were essentially identical to those of Wallenberg's syndrome. We propose that the oculomotor deficits in Wallenberg patients, whose lesions are in the lateral medulla, really result from chronic inhibition of caudal fastigial neurons. This inhibition ensues when the medullary lesion interrupts olivocerebellar fibers bound for the part of the vermal cortex afferent to the saccade-related fastigial neurons.