CEREBELLAR NUCLEI IN EYE MOVEMENT CONTROL AND ADAPTATION

University Of Washington, Seattle WA

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Abstract

Saccades, smooth pursuit, and vergence need to be extremely accurate to provide clear vision. Lesions of the cerebellum severely impair all three of these voluntary eye movements and abolish the ability to adapt eye movements when they are repeatedly inaccurate. We do not know what the cerebellum contributes to voluntary eye movements to make them accurate in the short-term and to adapt them in the long-term. The proposed research will study the contribution of one critical part of the cerebellum, the CFN, to voluntary eye movements. The CFN (caudal fastigial nucleus) send signals from the cerebellum to circuits that move the eyes. These signals make saccades and pursuit accurate by adding the proper horizontal component to each movement. We proposed that the CFN makes voluntary eye movements accurate in the long-term like it does in the short-term, i.e., by adding the necessary horizontal component. We will test this proposal by using single cell recording and temporary CFN lesions in behaving monkeys to determine if the CFN adds the horizontal component necessary to adapt saccades and pursuit. No previous work describes the specific role of any part of the cerebellum in adapting any voluntary movement, despite the act that adaptation is a function widely ascribed to the cerebellum. We will also use recording and temporary lesions to see if the CFN provides the appropriate horizontal component to cause the high speed vergence that occurs during saccades. Again, no previous work describes the neural mechanism of this saccadic-vergence though these movements are among the most common we make. The CFN has the appropriate anatomical connections and response properties to play a major role. Whatever its outcome, the proposed research will provide the first data on the neural mechanisms for adapting voluntary eye movements and for saccadic vergence. This data will certainly improve our understanding Of these functions and help us understand the adaptation and vergence deficits of human cerebellar patients. Our results may show specifically that the CFN provides the appropriate horizontal drive to support adaptation as well as saccades, pursuit, and saccadic-vergence. Thus, the CFN's long- and short-term effects on movement are simply two consequences of the same output. This unified view of two apparently different CFN functions would provide the first explicit model for understanding the role of other cerebellar output in controlling and adapting other voluntary movements.