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The Journal of Neurophysiology Vol. 86 No. 2 August 2001, pp. 651-661
Copyright ©2001 by the American Physiological Society
1Yerkes Regional Primate Research Center and Department of Neurology, Emory University, Atlanta, Georgia 30322; 2Department of Anatomy and Neuroscience, University of Texas Medical Branch, Galveston, Texas 77555; and 3Department of Physiology and Biophysics, University of Washington, Seattle, Washington 98195
Tusa, Ronald J.,
Michael J. Mustari,
Andrew
F. Burrows, and
Albert F. Fuchs.
Gaze-Stabilizing Deficits and Latent Nystagmus in Monkeys With
Brief, Early-Onset Visual Deprivation: Eye Movement Recordings. J. Neurophysiol. 86: 651-661, 2001. The
normal development and the capacity to calibrate gaze-stabilizing
systems may depend on normal vision during infancy. At the end of 1 yr
of dark rearing, cats have gaze-stabilizing deficits similar to that of
the newborn human infant including decreased monocular optokinetic
nystagmus (OKN) in the nasal to temporal (N-T) direction and decreased
velocity storage in the vestibuloocular reflex (VOR). The purpose of
this study is to determine to what extent restricted vision during the
first 2 mo of life in monkeys affects the development of
gaze-stabilizing systems. The eyelids of both eyes were sutured closed
in three rhesus monkeys (Macaca mulatta) at birth. Eyelids
were opened at 25 days in one monkey and 40 and 55 days in the other
two animals. Eye movements were recorded from each eye using scleral
search coils. The VOR, OKN, and fixation were examined at 6 and 12 mo of age. We also examined ocular alignment, refraction, and visual acuity in these animals. At 1 yr of age, visual acuity ranged from 0.3 to 0.6 LogMAR (20/40-20/80). All animals showed a defect in monocular
OKN in the N-T direction. The velocity-storage component of OKN (i.e.,
OKAN) was the most impaired. All animals had a mild reduction in VOR
gain but had a normal time constant. The animals deprived for 40 and 55 days had a persistent strabismus. All animals showed a nystagmus
similar to latent nystagmus (LN) in human subjects. The amount of LN
and OKN defect correlated positively with the duration of deprivation.
In addition, the animal deprived for 55 days demonstrated a pattern of
nystagmus similar to congenital nystagmus in human subjects. We found
that restricted visual input during the first 2 mo of life impairs
certain gaze-stabilizing systems and causes LN in primates.
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