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About the Authors:
Rosalyn M. Schneider
Affiliation: Veterans Affairs Medical Center, Case Western Reserve University, Cleveland, Ohio, United States of America
Matthew J. Thurtell
Affiliations Department of Ophthalmology & Visual Sciences, University of Iowa, Iowa City, Iowa, United States of America, Neurology Service and Center for the Prevention and Treatment of Visual Loss, Veterans Affairs Medical Center, Iowa City, Iowa, United States of America
Sylvia Eisele
Affiliation: Veterans Affairs Medical Center, Case Western Reserve University, Cleveland, Ohio, United States of America
Norah Lincoff
Affiliation: Jacobs Neurological Institute, State University of New York, Buffalo, New York, United States of America
Elisa Bala
Affiliation: Department of Ophthalmology, Cleveland Clinic Foundation, Cleveland, Ohio, United States of America
R. John Leigh
* E-mail: [email protected]
Affiliation: Veterans Affairs Medical Center, Case Western Reserve University, Cleveland, Ohio, United States of America
Introduction
Eye movements evolved to serve vision [1]. During locomotion, vestibular and visual tracking mechanisms act to stabilize the retinal image [2]. However, even while stationary, during attempted fixation of an earth-fixed target, small eye movements (microsaccades, drift, and tremor) are generated to prevent sensory adaptation, which would cause fading of the visual percept [3], [4]. In species with a fovea (a specialized area of the retina providing high visual acuity), saccades redirect the line of sight (the angle of gaze) toward features of interest [5].There is abundant evidence that the performance of these eye movements, including the vestibulo-ocular reflex [6], is optimized by visual feedback [7]–[9]. Such plastic-adaptive properties of eye movements in response to visual feedback constitute a type of motor learning, for which the cerebellum plays an important role [10].
One important component of gaze control is referred to as the neural integrator for eye movements, because it integrates premotor signals for saccades, pursuit, and vestibular inputs, which are velocity coded, into signals encoding eye position [2], [11]. This ocular motor integrator has been shown to depend on a distributed network of neurons, which include the medial vestibular nucleus and adjacent nucleus prepositus hypoglossi in the medulla, the interstitial nucleus of Cajal in the midbrain, and the vestibular cerebellum [12], [13]. The cellular mechanism by which neurons in the nucleus prepositus hypoglossi generate an eye position signal, has been identified as a cholinergic-mediated sustained depolarization [14]. Studies...