Kinematic and dynamic analyses were employed to study the effects of cerebellar lesions on conditioned and unconditioned nictitating membrane responses in the rabbit. It was found that conditioned responses acquired to an auditory stimulus accelerated in two bursts as indicated by two distinct peaks of acceleration. The second peak of acceleration was very weak during the early portions of conditioning but became a prominent feature of the conditioned response over 16 sessions of conditioning. The second peak of acceleration in the conditioned response was more sensitive to cerebellar damage than was the first peak. When lesions of the cerebellum permanently reduced the amplitude of conditioned responses, but did not affect their frequency, the second peak of acceleration was nearly abolished while the first peak was unaffected. When cerebellar lesions profoundly impaired both the amplitude and frequency of conditioned responses, large and permanent impairments occurred in both peaks of acceleration. Lesions of the anterior interpositus nucleus most severely impaired both peaks of acceleration in the conditioned response and significantly reduced the acceleration of unconditioned responses across a wide range of intensities of corneal air puff. The deficit in the acceleration of unconditioned responses became manifest only after membrane extension exceeded 0.12 mm. The impairment in the amplitude of the unconditioned response after cerebellar lesions more closely approximated the impairment in the amplitude of the conditioned response when the force-generating properties of the conditioned and unconditioned stimuli were equated. It was hypothesized, therefore, that one reason why conditioned responses are so easily disrupted by cerebellar lesions is because they are of low force and not simply because they are learned. It was proposed that the two peaks of acceleration that characterize the conditioned response represent the function of two distinct anatomical systems. The first, a short-latency system, initiates the response and is most likely mediated by circuits that traverse the pontomedullary reticular formation. The second, a longer-latency system, amplifies response amplitude and its neural basis remains to be elucidated. The two components of the conditioned response may reflect two sequential bursts of activity in the accessory abducens nucleus, the principal site of the motoneurons for the retractor bulbi muscle, or may reflect the synergistic activity of the accessory abducens nucleus and the motor nuclei of the other extraocular muscles. It was concluded that the vulnerability of the second component of the conditioned response to cerebellar damage reflects an important role for the cerebellum in modulating the degree to which long-latency neural systems contribute to the ongoing performance of learned and unlearned behaviors.