ABSTRACT
The experiment points to differential contributions of the cerebellum and basal ganglia in the performance of synchronized tapping. Lesions in the cerebellum appear to perturb the internal timing mechanism, manifest as an increase in the noise of this system. The mean error of the clock is likely to be proportional to the length of the timed interval, causing larger asynchronies for longer intervals. Pharmacological studies in humans and rats have suggested that the rate of an internal pacemaker may be altered by dopamine levels. All models of synchronization assume that the internal clock is engaged during paced and unpaced tapping. Estimates of clock and motor implementation variability were obtained through decomposition of the overall variability. The model postulates two component sources of noise: a central clock that provides the timing signals for the series of successive responses and a motor system that implements these responses.
