ORIENTING GAZE SHIFTS DURING MUSCIMOL INACTIVATION OF CAUDAL FASTIGIAL NUCLEUS IN THE CAT - I - GAZE DYSMETRIA

The cerebellar control of orienting behavior toward visual targets was studied in the head-unrestrained cat by analyzing the deficits of sac cadic gaze shifts after unilateral injection of muscimol in the caudal part of the fastigial nucleus (cFN). Gaze shifts are rendered strongl y inaccurate by muscimol cFN inactivation. The characteristics of gaze dysmetria are specific to the direction of the movement with respect to the inactivated cFN. Gaze shifts directed toward the injected side are hypermetric. Irrespective of their starting position, all these ip siversive gaze shifts overshoot the target by a constant horizontal er ror (or bias) to terminate at a ''shifted goal'' location. In particul ar, when gaze is directed initially at the future target's location, a response with an amplitude corresponding to the bias moves gaze away from the actual target. Additionally, when gaze is initially in betwee n the target and this shifted goal location, the response again is dir ected toward the latter. This deficit of ipsiversive gaze shifts is ch aracterized by a consistent increase in the y intercept of the relatio nship between horizontal gaze amplitude and horizontal retinal error. Slight increases in the slope sometimes are observed as well. Contrave rsive gaze shifts are markedly hypometric and, in contrast to ipsivers ive responses, they do not converge onto a shifted goal but rather und erestimate target eccentricity in a proportional way. This is reflecte d by a decrease in the slope of the relationship between horizontal ga ze amplitude and horizontal retinal error, with, for some experiments, a moderate change in the y-intercept value. The same deficits are obs erved in a different setup, which permits the control of initial gaze position. Correction saccades rarely are observed when visual feedback is eliminated on initiation of the primary orienting response; instea d, they occur frequently when the target remains visible. Like the pri mary contraversive saccades, they are hypometric and the ever-decreasi ng series of three to five correction saccades reduces the gaze fixati on error but often does not completely eliminate it. We measured the p osition of gaze after the final correction saccade and found that fixa tion of a visible target is still shifted toward the inactivated cFN b y 4.9 +/- 2.4 degrees. This fixation offset is correlated to, but on a verage 54% smaller than, the hypermetric bias of ipsiversive responses measured in the same experiments. In conclusion, the cFN contributes to the control of saccadic shifts of the visual axis toward a visual t arget. The hypometria of contraversive gaze shifts suggests a cFN role in adjusting a gain in the translation of retinal signals into gaze m otor commands. On the basis of the convergence of ipsiversive gaze shi fts onto a shifted goal, the straightness of gaze trajectory during th ese responses and the production of misdirected or inappropriately ini tiated responses toward this shifted goal, we propose that the cFN inf luences the processes that specify the goal of ipsiversive gaze shifts .