Variability in the effects of monocular deprivation on the optokinetic reflex of the non-deprived eye in the cat.

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.