Abstract
1. The inferior olive was destroyed by the drug 3‐acetylpyridine in brown rats. Spontaneous and optokinetic eye movements in response to constant‐velocity rotation (5‐80 deg/s) or sinusoidal oscillations (0.05 and 0.1 Hz with 15 deg/s peak velocity and 0.3, 0.5, 1.0 and 2 Hz with 5 deg/s peak velocity) of the visual surround were recorded 4‐6 days, 40‐50 days and 3‐4 months after the lesion using the magnetic search coil technique. 2. Persistent oculomotor deficits were observed in rats with a lesion of more than 97% of inferior olive neurones. In cases with a less complete lesion, no or only transient deficits were observed. In these latter cases the bulk of surviving neurones was located in the caudal half of the inferior olive, which includes the dorsal cap of Kooy. 3. Eye position holding after saccadic gaze shifts in the light was strongly deficient, showing pronounced postsaccadic centripetal drift for several hundred milliseconds. Similar deficits were observed in slow‐phase components following quick phases of optokinetic nystagmus. In the dark, eye position holding was also deficient. 4. Closed‐loop gains of optokinetic step responses obtained from rats with inferior olive lesions could be as good as those obtained from control animals. There was, however, a trend towards smaller gain values over the range of stimulus velocities tested. The duration of optokinetic after‐nystagmus was not changed. 5. The initial fast rise of slow‐phase velocity of optokinetic step responses was reduced by about 30‐50%, showing no recovery in the follow‐up experiments up to 3‐4 months after the lesion. 6. Optokinetic responses to sinusoidal oscillations of the visual surround exhibited an increasing drop in gain for frequencies between 0.1 to 0.5 Hz. In the range of 0.5‐2.0 Hz gain was only about 0.2 compared to 0.7‐0.8 in control animals. Phase lag of sinusoidal responses was shifted to larger values by about 25‐35 deg for frequencies increasing from 0.1 to 0.5 Hz. At 1.0 Hz phase shift was reduced to about 15 deg and at 2.0 Hz no significant change in phase was observed. Both gain and phase of sinusoidal responses showed some recovery when tested 3‐4 months after inferior olive lesion. 7. The results suggest that inferior olive lesions impair velocity‐to‐position integration, mainly as a consequence of the missing climbing fibre input to the cerebellar flocculi.(ABSTRACT TRUNCATED AT 400 WORDS)