Markner C, Hoffmann K P
Exp Brain Res. 1985;61(1):117-27. doi: 10.1007/BF00235627.
Six cats monocularly deprived by eye lid closure within the first week after birth showed the same deficits in the optokinetic reflex (OKR) when tested through the deprived eye as adults irrespective of whether the deprivation period was 6, 24 or 36 months. Closed loop gain (eye velocity/stimulus velocity) during temporo-nasal stimulus movement was below 0.8 and approached zero at stimulus velocities above 20 degrees/s. Naso-temporal stimulus movement was ineffective in eliciting OKR gain higher than 0.1 at velocities above 10 degrees/s. Different optokinetic deficits were found when the non-deprived eye was tested. In 3 cats OKR gain of the non-deprived eye was reduced with temporally directed stimulus movement when compared to normal whereas the gain of nasal OKR was uneffected. In these cats only monocular cells could be found in the nucleus of the optic tract (NOT), a pretectal cell aggregation involved in the optokinetic reflex pathway. In the other 3 cats the OKR of the non-deprived eye was not different from normal and could be elicited almost equally well in both directions. In these cats binocular cells were found in the NOT ipsilateral to the non-deprived eye. Again duration (6, 24 or 36 months) of monocular deprivation had no influence on this dichotomy. In a cat with asymmetric OKR of the non-deprived eye, the removal of the visual cortex ipsilateral to the non-deprived eye produced a small but significant gain decrease for temporal OKR of the non-deprived eye but no change when the deprived eye was tested. Visual cortex lesion ipsilateral to the deprived eye in the same cat had also no effect on the deprived eye's performance but reduced nasal OKR gain for the non-deprived eye at high velocities. The effects induced by long term monocular deprivation were not reversed after intensively forcing the use of the deprived eye by closing the non-deprived eye. Also enucleation of the deprived eye had no effect on the gain of the non-deprived eye. These optokinetic deficits are discussed in relation to functional changes in the NOT.
六只在出生后第一周通过眼睑闭合进行单眼剥夺的猫，成年后通过被剥夺的眼睛测试时，无论剥夺期是6个月、24个月还是36个月，其视动反射（OKR）都表现出相同的缺陷。在颞鼻向刺激运动期间，闭环增益（眼球速度/刺激速度）低于0.8，在刺激速度高于20度/秒时接近零。在速度高于10度/秒时，鼻颞向刺激运动在引发高于0.1的OKR增益方面无效。当测试未被剥夺的眼睛时，发现了不同的视动缺陷。在3只猫中，与正常情况相比，未被剥夺的眼睛在颞向刺激运动时OKR增益降低，而鼻侧OKR增益未受影响。在这些猫中，仅在视束核（NOT）中发现了单眼细胞，视束核是一个参与视动反射通路的顶盖前细胞聚集区。在另外3只猫中，未被剥夺的眼睛的OKR与正常情况无异，并且在两个方向上引发的效果几乎相同。在这些猫中，在未被剥夺的眼睛同侧的视束核中发现了双眼细胞。同样，单眼剥夺的持续时间（6个月、24个月或36个月）对这种二分法没有影响。在一只未被剥夺的眼睛的OKR不对称的猫中，切除未被剥夺的眼睛同侧的视觉皮层，未被剥夺的眼睛的颞侧OKR增益出现小幅但显著的下降，但测试被剥夺的眼睛时没有变化。在同一只猫中，被剥夺的眼睛同侧的视觉皮层损伤对被剥夺的眼睛的表现也没有影响，但在高速时降低了未被剥夺的眼睛的鼻侧OKR增益。在通过闭合未被剥夺的眼睛来强烈强迫使用被剥夺的眼睛后，长期单眼剥夺所诱导的效应并未逆转。此外，摘除被剥夺的眼睛对未被剥夺的眼睛的增益也没有影响。本文结合视束核中的功能变化对这些视动缺陷进行了讨论。
