ROLE OF THE NUCLEUS OF THE OPTIC TRACT OF MONKEYS IN OPTOKINETIC NYSTAGMUS AND OPTOKINETIC AFTER-NYSTAGMUS
ROLE OF THE NUCLEUS OF THE OPTIC TRACT OF MONKEYS IN OPTOKINETIC NYSTAGMUS AND OPTOKINETIC AFTER-NYSTAGMUS
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DOI：
10.1016/0006-8993(88)90665-8
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发表时间：
1988-11-22
期刊：
影响因子：
2.9
通讯作者：
IKARASHI, T
中科院分区：
文献类型：
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作者：
KATO, I;HARADA, K;IKARASHI, T
以前的实验表明，单方面损害的视束核（NOT）在fascicularis猴导致选择性的损失视动性眼震（OKN）对损害的一面。这可能表明，猴子的NOT和非灵长类动物一样，代表了基本水平视动路径中的第一个中继站。然而，这只猴子并没有表现出对刺激速度的阶跃反应的OKN速度的快速上升。在本实验中，我们观察了6只棕色猕猴的NOT损伤对OKN的快速和缓慢上升以及视动性后眼球震颤（OKAN）的影响。6只猴中3只全部为NOT病变，病变侧无OKN或OKAN慢相速度的缓慢上升。在其余3只部分NOT病变的猴子中，缓慢上升的OKN和OKAN慢相速度选择性地向病变侧降低。在这4只猴子的病变局限于外侧部分的前顶盖，OKN速度的快速上升保持不变，而在其余的两个病变足够大，延伸到内侧部分的前顶盖附近的核的后连合，OKN速度的快速上升减少。在剩下的2只猴中，其NOT仅表面受损，OKN的所有组分均正常。其他视觉诱导的眼球运动正常。在所有的猴子，除了一个谁有显着的自发性眼震，前庭眼震的峰值速度不受影响后NOT病变。这些发现表明，速度储存机制的电荷动力学分别受到NOT病变的影响：OKN和OKAN被取消，但前庭眼球震颤保持不受影响。
A previous experiment disclosed that unilateral lesions of the nucleus of the optic tract (NOT) in the fascicularis monkey resulted in selective loss of optokinetic nystagmus (OKN) towards the lesioned side. This may suggest that the NOT in monkeys, as in non-primates, represents the first relay station in the basic horizontal optokinetic path. This monkey, however, did not show a rapid rise in OKN velocity in response to steps in stimulus velocity. In the present experiments, effects of NOT lesions upon both the rapid and the slow rise of OKN as well as optokinetic after-nystagmus (OKAN) were examined in 6 fuscata monkeys. In 3 with total NOT lesions of 6 monkeys, none of the slow rise OKN or OKAN slow phase velocity were produced towards the lesioned side. In one of the remaining 3 monkeys with partial NOT lesions, a slow rise OKN and OKAN slow phase velocity were selectively reduced towards the lesioned side. In 2 of these 4 monkeys whose lesions were localized in the lateral portions of the pretectum, rapid rise in OKN velocity remained unchanged, whereas in the remaining two whose lesions were large enough to extend into the medial portions of the pretectum near the nucleus of the posterior commissure, rapid rise in OKN velocity was reduced. In the remaining 2 monkeys whose NOT was only superficially damaged, all components of OKN were normal. Other visually induced eye movements were normal. In all monkeys except for one who had marked spontaneous nystagmus, the peak velocity of vestibular nystagmus was not affected after NOT lesions. These findings indicate that the dynamics of the charge of the velocity storage mechanism is separately influenced by NOT lesions: OKN and OKAN are abolished, but vestibular nystagmus remains unaffected.