Magnocellular or parvocellular lesions in the lateral geniculate nucleus of monkeys cause minor deficits of smooth pursuit eye movements.

The effects of unilateral LGN lesions, made with ibotenic acid, on smooth pursuit eye movements were studied in two monkeys (Macaca nemestrina). Both monkeys received unilateral magnocellular (M-) layer lesions 18 months before the study and one monkey received a parvocellular (P-) lesion during the study on the side opposite the magnocellular lesion. The lesions did not affect the accuracy of saccades to stationary or moving targets, but the latencies of saccades to targets in the M-layer lesioned hemifields were significantly longer. Neither M- nor P-layer lesions affected the earliest interval (0-50 msec) of pursuit initiation, but during later intervals (50-150 msec), eye acceleration was less for pursuit initiation in the lesioned hemifield compared to the control hemifield. M-layer lesions created larger deficits in ocular acceleration than P-layer lesions. All deficits, however, were relatively small and accurate pursuit speeds were achieved near the time of the initial "catch-up" saccade. If both M and P layers representing the same part of the visual field were destroyed, the monkey was unable to locate the target or initiate smooth pursuit eye movements. We conclude that smooth pursuit initiation receives contributions from both the M- and P-layers of the LGN and either of these inputs can support pursuit initiation.