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Deficits in Saccades and Fixation During Muscimol Inactivation of the Caudal Fastigial Nucleus in the Rhesus Monkey

¹Department of Psychology, University of Pennsylvania, Philadelphia, Pennsylvania 19104; ²Department of Neuroscience, Baylor College of Medicine, Houston, Texas 77030; and ³Equipe Dynamique de la Vision et de l’Action, Institut de Neurosciences Cognitives de la Méditerranée, Unité Mixte de Recherche 6193 Centre National de la Recherche Scientifique—Université de la Méditerranée, 13402 Marseille, France

Submitted 11 December 2003; accepted in final form 28 June 2004

The caudal fastigial nucleus (cFN) is a major nucleus by which the cerebellum influences the accuracy of saccades. In head-restrained monkeys generating saccades from a fixation light-emitting diode (LED) toward a flashed target LED, we analyzed the effects of unilateral pharmacological inactivation of cFN on horizontal, vertical, and oblique saccades. When animals were viewing the fixation LED, usually after one or more correction saccades, the positions of the eyes were slightly offset in comparison with the positions maintained before the injection (average offset = 1.1°). The offset was ipsilateral to the injected side and did not depend on the target location. The horizontal component of all ipsilesional saccades was hypermetric and associated with a 32–42% increase in the amplitude of the deceleration displacement without significant change in the amplitude of the acceleration displacement. The horizontal component of all contralesional saccades was hypometric and associated with a decrease in the peak velocity and in the acceleration amplitude (30–35% decrease) without significant change in the deceleration amplitude. The amplitude of vertical saccades was not systematically affected, but their trajectory was always deviated toward the injected side. They missed the target with an error that depended on saccade duration or amplitude. If any, the effects of muscimol injections on the vertical component of oblique saccades were very small. The changes in fixation and the dysmetria are both viewed as consequences of an impairment in the cFN bilateral influence on the burst neurons located in the left and right brain stem.

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