The characteristics and neuronal substrate of saccadic eye movement plasticity

Abstract

Saccadic eye movements are shifts in the direction of gaze that rapidly and accurately aim the fovea at targets of interest. Saccades are so brief that visual feedback cannot guide them to their targets. Therefore, the saccadic motor command must be accurately specified in advance of the movement and continually modified to compensate for growth, injury, and aging, which otherwise would produce dysmetric saccades. When a persistent dysmetria occurs in subjects with muscle weakness or neural damage or is induced in normal primates by the surreptitious jumping of a target forward or backward as a saccade is made to acquire the target, saccadic amplitude changes to reduce the dysmetria. Adaptation of saccadic amplitude or direction occurs gradually and is retained in the dark, thus representing true motor plasticity. Saccadic adaptation is more rapid in humans than in monkeys, usually is incomplete in both species, and is slower and less robust for amplitude increases than decreases. Adaptation appears to be motor rather than sensory. In humans, adaptation of saccades that would seem to require more sensory-motor processing does not transfer to saccades that seem to require less, suggesting the existence of distributed adaptation loci. In monkeys, however, transfer from more simple to more complex saccades is robust, suggesting a common adaptation site. Neurophysiological data from both species indicate that the oculomotor cerebellum is crucial for saccadic adaptation. This review shows that the precise, voluntary behaviors known as saccadic eye movements provide an alternative to simple reflexes for the study of the neuronal basis of motor learning.