Upadhyaya Suraj, Meng Hui, Das Vallabh E
College of Optometry, University of Houston, Houston, Texas.
College of Optometry, University of Houston, Houston, Texas
J Neurophysiol. 2017 Mar 1;117(3):1281-1292. doi: 10.1152/jn.00437.2016. Epub 2016 Dec 28.
Disruption of binocular vision during the critical period for development leads to eye misalignment in humans and in monkey models. We have previously suggested that disruption within a vergence circuit could be the neural basis for strabismus. Electrical stimulation in the rostral superior colliculus (rSC) leads to vergence eye movements in normal monkeys. Therefore, the purpose of this study was to investigate the effect of SC stimulation on eye misalignment in strabismic monkeys. Electrical stimulation was delivered to 51 sites in the intermediate and deep layers of the SC (400 Hz, 0.5-s duration, 10-40 μA) in 3 adult optical prism-reared strabismic monkeys. Scleral search coils were used to measure movements of both eyes during a fixation task. Staircase saccades with horizontal and vertical components were elicited by stimulation as predicted from the SC topographic map. Electrical stimulation also resulted in significant changes in horizontal strabismus angle, i.e., a shift toward exotropia/esotropia depending on stimulation site. Electrically evoked saccade vector amplitude in the two eyes was not significantly different ( > 0.05; paired -test) but saccade direction differed. However, saccade disconjugacy accounted for only ~50% of the change in horizontal misalignment while disconjugate postsaccadic movements accounted for the other ~50% of the change in misalignment due to electrical stimulation. In summary, our data suggest that electrical stimulation of the SC of strabismic monkeys produces a change in horizontal eye alignment that is due to a combination of disconjugate saccadic eye movements and disconjugate postsaccadic movements. Electrical stimulation of the superior colliculus in strabismic monkeys results in a change in eye misalignment. These data support the notion of developmental disruption of vergence circuits leading to maintenance of eye misalignment in strabismus.
在发育关键期双眼视觉的破坏会导致人类和猴子模型出现眼位偏斜。我们之前曾提出,聚散回路内的破坏可能是斜视的神经基础。在正常猴子中,对嘴侧上丘(rSC)进行电刺激会引发聚散眼球运动。因此,本研究的目的是探究刺激上丘对斜视猴子眼位偏斜的影响。对3只成年光学棱镜饲养的斜视猴子的上丘中间层和深层的51个位点进行电刺激(400Hz,持续0.5秒,10 - 40μA)。在固定任务期间,使用巩膜搜索线圈测量双眼的运动。如根据上丘地形图所预测的那样,刺激引发了具有水平和垂直分量的阶梯状扫视。电刺激还导致水平斜视角度发生显著变化,即根据刺激位点向外斜视/内斜视转变。双眼的电诱发扫视矢量幅度无显著差异(>0.05;配对t检验),但扫视方向不同。然而,扫视非共轭性仅占水平眼位偏斜变化的约50%,而非共轭的扫视后运动占电刺激引起的眼位偏斜变化的另外约50%。总之,我们的数据表明,对斜视猴子的上丘进行电刺激会导致水平眼位对准发生变化,这是由于非共轭扫视眼球运动和非共轭扫视后运动共同作用的结果。对斜视猴子的上丘进行电刺激会导致眼位偏斜发生变化。这些数据支持了聚散回路发育破坏导致斜视中眼位偏斜持续存在这一观点。