Saccades are the rapid eye movements used to change visual fixation. These eye movements are very accurate and end without drift. Our previous experiments have shown that the brain controls saccadic accuracy and 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 in primates showed that the cerebellum was required for altering the gain and time constants of the neural components of saccadic innervation. After ablation of the midline vermis and fastigial nuclei saccades became hypermetric, and the adaptive control of saccadic accuracy was lost. After bilateral flocculectomy, monkeys developed post-saccadic ocular drift and became insensitive to optically-imposed retinal slip. The current work studies two aspects of saccadic adaptation. First, we are extending the work on post-saccadic drift suppression to human subjects. We have already found that human subjects, like monkeys, respond to optically-induced post-saccadic slip by developing post-saccadic ocular drift. In addition, this mechanism appears binocular, and can not adjust the innervation to the two eyes differently. The second study attempts to determine the neural mechanisms underlying adaptive control of saccadic accuracy. By comparing details of the saccadic waveform before and after adaptation with possible models for saccade generation, it can be shown that saccadic accuracy must be controlled upstream from the superior colliculus, by changing the size of the saccadic command. Preliminary evidence suggests that the innervation changes come from a second, parallel pathway that contributes to the main visual pathway of the saccade command.
