Deficits in Orienting Gaze Shifts during Muscimol Inactivation of the
Caudal Fastigial Nucleus in the Cat. I. Gaze Dysmetria.
Laurent Goffart and Denis P‚lisson.
Vision et Motricit‚, INSERM U 94, 16 avenue Doyen L‚pine, 69500 Bron
(France).
APStracts 4:367N, 1997.
ABSTRACT
The cerebellar control of orienting behavior toward visual targets was studied
in the head-unrestrained cat, by analyzing the deficits of saccadic gaze
shifts following unilateral injection of muscimol in the caudal part of the
fastigial nucleus (cFN). Gaze shifts are rendered strongly inaccurate by
muscimol cFN inactivation. The characteristics of gaze dysmetria are specific
to the direction of the movement with respect to the inactivated cFN. Gaze
shifts directed toward the injected side are hypermetric. Irrespective of
their starting position, all these ipsiversive gaze shifts overshoot the
target by a constant horizontal error (or bias) to terminate at a "shifted
goal" location. In particular, when gaze is initially directed at the future
target's location, a response with an amplitude corresponding to the bias
moves gaze away from the actual target. Additionally, when gaze is initially
in between the target and this "shifted goal" location, the response is again
directed toward the latter. This deficit of ipsiversive gaze shifts is
characterized by a consistent increase in the y-intercept of the relationship
between horizontal gaze amplitude and horizontal retinal error. Slight
increases in the slope are sometimes observed as well. Contraversive gaze
shifts are markedly hypometric and, in contrast to ipsiversive responses, they
do not converge onto a "shifted goal" but rather underestimate target
eccentricity in a proportional way. This is reflected by a decrease in the
slope of the relationship between horizontal gaze amplitude and horizontal
retinal error, with, for some experiments, a moderate change in the y-
intercept value. The same deficits are observed in a different setup that
permits the control of initial gaze position. Correction saccades are rarely
observed when visual feedback is eliminated upon initiation of the primary
orienting response; instead, they occur frequently when the target remains
visible. Like the primary contraversive saccades, they are hypometric and the
ever- decreasing amplitude of a series of 3-5 correction saccades reduce the
gaze fixation error, but often do not completely eliminate it. We measured the
position of gaze after the final correction saccade and found that fixation of
a visible target is still shifted toward the inactivated cFN by 4.9 +/- 2.4
deg. This fixation offset is correlated to, but on average 54 % smaller than,
the hypermetric bias of ipsiversive responses measured in the same
experiments. In conclusion, the cFN contributes to the control of saccadic
shifts of the visual axis toward a visual target. The hypometria of
contraversive gaze shifts suggests a cFN role in adjusting a gain in the
translation of retinal signals into gaze motor commands. Based on the
convergence of ipsiversive gaze shifts onto a "shifted goal", the straightness
of gaze trajectory during these responses, and the production of misdirected
or inappropriately-initiated responses toward this "shifted goal", we propose
that the cFN influences the processes that specify the goal of ipsiversive
gaze shifts.
Received 18 February 1997; accepted in final form 8 December 1997.
APS Manuscript Number J144-7.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 12 December 1997