A neuronal process for adaptive control of primate saccadic system.

Abstract

In 1980, Dr. Optican established the existence of an adaptive plasticity of saccades and its dependence on the cerebellum with Dr. Robinson. The advantage of saccades is that the neuronal mechanisms underlying their generation have been well established. This knowledge allows us to identify the neuronal elements that participate in saccade adaptation. Briefly, the superior colliculus (SC) produces a saccade command signal, which reaches motoneurons in the abducens nucleus via the brainstem burst generator. The SC saccade command also is sent to the oculomotor vermis (OMV), a saccade-related area of the cerebellar cortex, and finally converges on the same motoneurons via the caudal fastigial nucleus (cFN) and inhibitory burst neurons (IBN). During adaptation, the saccade-related burst of SC neurons does not change; however, the activity of the cerebellum and its downstream targets do. We demonstrate that the SC is the source of the error signal to the OMV, and the error signal increases the probability of complex spike occurrence and decreases simple spike activity in the OMV. This decrease, in turn, is delivered through the cFN and IBN neurons to decrease motoneuron activity and hence saccade amplitude.