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J Neurophysiol 79: 1959-1976, 1998;
0022-3077/98 $5.00
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The Journal of Neurophysiology Vol. 79 No. 4 April 1998, pp. 1959-1976
Copyright ©1998 The American Physiological Society

Orienting Gaze Shifts During Muscimol Inactivation of Caudal Fastigial Nucleus in the Cat. II. Dynamics and Eye-Head Coupling

Laurent Goffart, Denis Pélisson, and Alain Guillaume

Espace et Action, Institut National de la Santé et de la Recherche Médicale U94, 69500 Bron, France

Goffart, Laurent, Denis Pélisson, and Alain Guillaume. Orienting gaze shifts during muscimol inactivation of caudalfastigial nucleus in the cat. II. Dynamics and eye-head coupling. J. Neurophysiol. 79: 1959-1976, 1998. We have shown in the companion paper that muscimol injection in the caudal part of the fastigial nucleus (cFN) consistently leads to dysmetria of visually triggered gaze shifts that depends on movement direction. Based on the observations of a constant error and misdirected movements toward the inactivated side, we have proposed that the cFN contributes to the specification of the goal of the impending ipsiversive gaze shift. To test this hypothesis and also to better define the nature of the hypometria that affects contraversive gaze shifts, we report in this paper on various aspects of movement dynamics and of eye/head coordination patterns. Unilateral muscimol injection in cFN leads to a slight modification in the dynamics of both ipsiversive and contraversive gaze shifts (average velocity decrease = 55°/s). This slowing in gaze displacements results from changes in both eye and head. In some experiments, a larger gaze velocity decrease is observed for ipsiversive gaze shifts as compared with contraversive ones, and this change is restricted to the deceleration phase. For two particular experiments testing the effect of visual feedback, we have observed a dramatic decrease in the velocity of ipsiversive gaze shifts after the animal had received visual information about its inaccurate gaze responses; but virtually no change in hypermetria was noted. These observations suggest that there is no obvious causal relationship between changes in dynamics and in accuracy of gaze shifts after muscimol injection in the cFN. Eye and head both contribute to the dysmetria of gaze. Indeed, muscimol injection leads to parallel changes in amplitude of both ocular and cephalic components. As a global result, the relative contribution of eye and head to the amplitude of ipsiversive gaze shifts remains statistically indistinguishable from that of control responses, and a small (1.6°) increase in the head contribution to contraversive gaze shifts is found. The delay between eye and head movement onsets is increased by 7.3 ± 7.4 ms for contraversive and decreased by 8.3 ± 10.1 ms for ipsiversive gaze shifts, corresponding respectively to an increased or decreased lead time of head movement initiation. The modest changes in gaze dynamics, the absence of a link between eventual dynamics changes and dysmetria, and a similar pattern of eye-head coordination to that of control responses, altogether are compatible with the hypothesis that the hypermetria of ipsiversive gaze shifts results from an impaired specification of the metrics of the impending gaze shift. Regarding contraversive gaze shifts, the weak changes in head contribution do not seem to reflect a pathological coordination between eye and head but would rather result from the tonic deviations of gaze and head toward the inactivated side. Hence, our data suggest that the hypometria of contraversive gaze shifts also might result largely from an alteration of processes that specify the goal rather than the on-going trajectory, of saccadic gaze shifts.




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