Cheron G, Gillis P, Godaux E
J Physiol. 1986 Mar;372:95-111. doi: 10.1113/jphysiol.1986.sp015999.
The effects of bilateral lesions within and around the prepositus hypoglossi (p.h.) nuclei on the optokinetic system were studied. The pure optokinetic nystagmus (o.k.n.) was evoked by a step of velocity (60 deg/s, 30 s duration) of the surrounding. The visual-vestibular interaction was investigated by measuring the gain and phase of the vestibulo-ocular reflex (v.o.r.) as a function of frequency before and after lesion under three different conditions of testing: basic v.o.r. tested in the dark, v.o.r. tested in the light and v.o.r. suppressed by vision. The tested amplitude was +/- 20 deg. A posterior vermectomy was performed for controls in two cats. A bilateral electrolytic p.h. lesion including the rostral pole of this nucleus was added to the posterior vermectomy in three cats. A lesion similar but sparing the rostral pole of the nucleus was carried out in three other cats. In one cat a bilateral electrolytic lesion of the medial vestibular nuclei (m.v.n.) was combined with a posterior vermectomy. In two cats the medulla was cut on the mid line after a posterior vermectomy. The posterior vermectomy affected neither the optokinetic response nor the visual-vestibular interactions. In cats where p.h. lesion included its rostral pole and in the cat with m.v.n. lesion, all the tested optokinetic effects (step o.k.n., and visual-vestibular interactions) were abolished. In the three cats where p.h. lesion spared its rostral pole, the optokinetic effects were quite normal in one cat, mildly reduced in the second one, and seriously affected but not completely abolished in the third one. The surgical cut of the medulla on the mid line did not dramatically disturb the various optokinetic effects. The most marked deficit was the loss of the optokinetic after-nystagmus (o.k.a.n.). From the comparison of these results with the neuroanatomical data and with the Robinson's model concerning the optokinetic processing, it was suggested that: (a) the rostral p.h. could be the location of the o.k.n. integrator or could be an essential link on the o.k.n. pathway, (b) the posterior four-fifths of the p.h. could not be an essential relay on the o.k.n. pathway, (c) the loss of o.k.a.n. after mid-line lesion could be due to the interruption of the positive feed-back loop formed by the reciprocal inhibitory connexions between the two m.v.n.
研究了双侧舌下前置核（p.h.）及其周围区域的损伤对视动系统的影响。通过使周围环境以60度/秒的速度阶跃变化（持续30秒）来诱发纯视动性眼震（o.k.n.）。在三种不同的测试条件下，通过测量前庭眼反射（v.o.r.）的增益和相位作为频率的函数，来研究视觉-前庭相互作用：在黑暗中测试的基本v.o.r.、在光照下测试的v.o.r.以及视觉抑制的v.o.r.。测试幅度为±20度。对两只猫进行后蚓部切除术作为对照。在三只猫中，在后蚓部切除术后增加双侧电解性p.h.损伤，包括该核的嘴侧极。在另外三只猫中进行了类似但保留核嘴侧极的损伤。在一只猫中，将双侧内侧前庭核（m.v.n.）的电解性损伤与后蚓部切除术相结合。在两只猫中，在后蚓部切除术后沿中线切断延髓。后蚓部切除术既不影响视动反应，也不影响视觉-前庭相互作用。在p.h.损伤包括其嘴侧极的猫以及m.v.n.损伤的猫中，所有测试的视动效应（阶跃o.k.n.和视觉-前庭相互作用）均被消除。在p.h.损伤保留其嘴侧极的三只猫中，一只猫的视动效应完全正常，第二只猫轻度降低，第三只猫严重受损但未完全消除。沿中线对延髓进行手术切断并未显著干扰各种视动效应。最明显的缺陷是视动性眼震后眼震（o.k.a.n.）的丧失。通过将这些结果与神经解剖学数据以及关于视动处理的罗宾逊模型进行比较，提示：（a）嘴侧p.h.可能是o.k.n.积分器的位置，或者可能是o.k.n.通路中的关键环节；（b）p.h.的后五分之四不可能是o.k.n.通路中的关键中继；（c）中线损伤后o.k.a.n.的丧失可能是由于两个m.v.n.之间的相互抑制性连接形成的正反馈回路中断所致。
