Saccades are the rapid eye movements used to change visual fixation. These eye movements are very fast yet they end abruptly, i.e., the eyes do not drift at the end of a saccade. This lack of post-saccadic drift is essential for good visual acuity after a saccade. Previous experiments in this laboratory have shown that the brain actively suppresses post-saccadic drift by altering the levels of innervation sent to the muscles during and after a saccade. The adaptive mechanism for suppression of post-saccadic drift is sensitive to optically-imposed post-saccadic retinal slip. Our previous work showed that a central neural mechanism attempted to compensate for this post-saccadic retinal slip by altering the gain and time constants of the neural components of saccadic innervation. This altered innervation led to a post-saccadic ocular drift that lessened the amount of post-saccadic retinal slip. We have previously shown that this central adaptive mechanism was dependent upon the cerebellum for its proper function. After a complete cerebellectomy, monkeys developed post-saccadic ocular drift, and were unable to compensate for post-saccadic retinal slip. The present work has now shown that the site of this functional dependency can be further localized to the cerebellar flocculi and paraflocculi. After bilateral flocculectomy, monkeys developed post-saccadic ocular drift. When rpesented with optically-imposed post-saccadic retinal slip, the animals were only able to alter their saccadic innervations a little. These post-flocculectomy alterations were not large enough to compensate for the retinal slip. Furthermore, this ability was asymmetric, with reductions in gain being larger than increases.
