Changes in initiation of orienting gaze shifts after muscimol inactivation of the caudal fastigial nucleus in the cat.

1. The production of a goal-directed saccadic gaze shift involves the specification of movement amplitude and direction, and the decision to trigger the movement. Behavioural and neurophysiological data suggest that these two functions involve separate processes which may interact. 2. The medio-posterior cerebellar areas are classically assigned a major contribution to the control of saccade metrics, and previous cerebellar lesion studies have revealed marked dysmetria of visually triggered gaze shifts. In contrast, these studies did not provide evidence for a cerebellar role in saccadic initiation. 3. In the present study, we investigated in the head-unrestrained cat the deficits in both the initiation and the metrics control of saccadic gaze shifts following pharmacological inactivation of the caudal part of the fastigial nucleus (cFN). 4. After cFN inactivation, latencies for contraversive gaze shifts increased to about 137 +/- 28% of normal, and latencies for ipsiversive gaze shifts decreased to about 84 +/- 8% of normal. Similar changes in head movement latency were observed, such that the temporal coupling between eye and head components remained largely unaffected. 5. Contraversive gaze shifts were more hypometric as their latency increased. In contrast, the degree of hypermetria in ipsiversive gaze shifts was unrelated to latency. 6. These results suggest a functional role of the medio-posterior cerebellum in gaze shift initiation and in storing information about the target location and/or the desired gaze shift amplitude.