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The Journal of Neurophysiology Vol. 84 No. 1 July 2000, pp. 216-235
Copyright ©2000 by the American Physiological Society
Howard Hughes Medical Institute, Department of Physiology, W. M. Keck Foundation Center for Integrative Neuroscience, and Neuroscience Graduate Program, University of California, San Francisco, California 94143
Churchland, Mark M. and
Stephen G. Lisberger.
Apparent Motion Produces Multiple Deficits in Visually Guided
Smooth Pursuit Eye Movements of Monkeys. J. Neurophysiol. 84: 216-235, 2000. We used apparent motion
targets to explore how degraded visual motion alters smooth pursuit eye
movements. Apparent motion targets consisted of brief stationary
flashes with a spatial separation (
x), temporal
separation (
t), and apparent target velocity equal to
x/
t. Changes in pursuit initiation
were readily observed when holding target velocity constant and
increasing the flash separation. As flash separation increased, the
first deficit observed was an increase in the latency to peak eye
acceleration. Also seen was a paradoxical increase in initial eye
acceleration. Further increases in the flash separation produced larger
increases in latency and resulted in decreased eye acceleration. By
varying target velocity, we were able to discern that the visual inputs driving pursuit initiation show both temporal and spatial limits. For
target velocities above 4-8°/s, deficits in the initiation of
pursuit were seen when
x exceeded 0.2-0.5°, even
when
t was small. For target velocities below
4-8°/s, deficits appeared when
t exceeded 32-64
ms, even when
x was small. Further experiments were
designed to determine whether the spatial limit varied as retinal and
extra-retinal factors changed. Varying the initial retinal position of
the target for motion at 18°/s revealed that the spatial limit
increased as a function of retinal eccentricity. We then employed
targets that increased velocity twice, once from fixation and again
during pursuit. These experiments revealed that, as expected, the
spatial limit is expressed in terms of the flash separation on the
retina. The spatial limit is uninfluenced by either eye velocity or the
absolute velocity of the target. These experiments also demonstrate
that "initiation" deficits can be observed during ongoing pursuit,
and are thus not deficits in initiation per se. We conclude that such
deficits result from degradation of the retino-centric motion signals
that drive pursuit eye acceleration. For large flash separations, we
also observed deficits in the maintenance of pursuit: sustained eye
velocity failed to match the constant apparent target velocity.
Deficits in the maintenance of pursuit depended on both target velocity and
t and did not result simply from a failure of
degraded image motion signals to drive eye acceleration. We argue that
such deficits result from a low gain in the eye velocity memory that
normally supports the maintenance of pursuit. This low gain may appear because visual inputs are so degraded that the transition from fixation
to tracking is incomplete.
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