The Journal of Neurophysiology Vol. 78 No. 2 August 1997, pp. 848-859
Copyright ©1997 The American Physiological Society

Participation of Caudal Fastigial Nucleus in Smooth Pursuit Eye Movements. II. Effects of Muscimol Inactivation

Farrel R. Robinson¹, Andreas Straube², and Albert F. Fuchs¹

¹ Department of Physiology and Biophysics and Regional Primate Research Center, University of Washington, Seattle, Washington 98195-7330; and ² Department of Neurology, Grosshadern Clinic, University of Munich, 81377 Munich, Germany

Robinson, Farrel, R., Andreas Straube, and Albert F. Fuchs. Participation of the caudal fastigial nucleus in smooth pursuit eye movements. II. Effects of muscimol inactivation. J. Neurophysiol. 78: 848-859, 1997. We studied the effect of temporarily inactivating the caudal fastigial nucleus (CFN) in three rhesus macaques trained to make smooth pursuit eye movements. We injected the -aminobutyric acid A agonist muscimol into one or both CFNs where we had recorded pursuit-related neurons a few minutes earlier. Inactivating the CFN on one side impaired pursuit in one monkey so severely that it could not follow step-ramp targets moving at 20°/s, the target velocity that we used to test the other two monkeys. We tested this monkey with targets moving at 10°/s. In all three monkeys, unilateral CFN inactivation either increased the acceleration of ipsilateral step-ramp pursuit (in 2 monkeys, to 144 and 220% of normal) or decreased the acceleration of contralateral pursuit (in 1 monkey, to 71% of normal). Muscimol injected into both CFNs in two of the monkeys left both ipsilateral and contralateral acceleration nearly normal in both monkeys (101% of normal). Unilateral CFN inactivation also impaired the velocity of maintained pursuit as the monkeys tracked a target moving at a constant velocity or oscillating sinusoidally. Averaged across both types of movements in all three monkeys, gains for ipsilateral, contralateral, upward, and downward pursuit were 94, 67, 84, and 73% of normal, respectively. Unilateral CFN inactivation also impaired the monkeys' ability to suppress their vestibuloocular reflex (VOR). Averaged across the two monkeys VOR gain during suppression increased from 0.06 to 0.25 during yaw rotation and from 0.21 to 0.59 during pitch rotation. Bilateral CFN inactivation reduced pursuit gains in all directions more than unilateral injection did. In the two monkeys tested, ipsilateral, contralateral, upward, and downward gains went from 94, 86, 85, and 74% of normal, respectively, after we inactivated one CFN to 88, 73, 80, and 64% of normal after we also inactivated the second CFN. We can explain many, but not all, of the effects of CFN activation on smooth pursuit with the behavior of CFN neurons, and the assumption that the activity of each CFN neuron helps drive pursuit movements in the direction that best activates that neuron. We conclude that the CFN, like the flocculus-ventral paraflocculus, is a cerebellar region involved in control of smooth pursuit.

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