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Unilateral cerebellar lesions abolished the occurrence of ipsilateral conditioned nictitating membrane responses during the 285 msec interval between onset of the conditioned and unconditioned stimuli on paired trials. This effect was obtained in 15 animals sustaining damage to the dorsolateral aspects of the interpositus nucleus and the adjoining white matter. However, conditioned responses did occur during the 800 msec observation interval employed on tone-alone test trials, and these responses exhibited the classic performance deficits normally associated with cerebellar damage: a low frequency of occurrence (14%, as compared with 96% before the lesion); a 3.1 mm decrease in amplitude; a 236 msec increase in onset latency; a 563 msec increase in latency of peak amplitude; and a 327 msec increase in rise time. Four of the 15 animals failed to demonstrate greater than 5% responding during the test trials. These performance deficits were not specific to the learned, conditioned response. Unconditioned responses were also reduced in frequency and increased in latency of peak amplitude and rise time, especially when elicited at lower air-puff intensities. These deficits in the unconditioned response were observed in animals that failed to exhibit conditioned responses on either paired or test trials, as well as in animals demonstrating conditioned responses only during test trials. We conclude that the cerebellum has a general role in regulating the nictitating membrane reflex so that deficits in learned responses observed after cerebellar lesions are secondary to a broader deficit in performance. The performance deficits appear to consist of a sensory component, as reflected by an increase in stimulus threshold for elicitation of the nictitating membrane reflex, and a motor component, as reflected by the altered topography of the evoked response. The results of this study thus reaffirm the role of the cerebellum in regulating the sensorimotor processes necessary for the optimal performance of both conditioned and unconditioned responses and extends this role to the expression of a simple cranial nerve reflex.

Cerebellar lesions and the nictitating membrane reflex: performance deficits of the conditioned and unconditioned response