Optokinetic reflex in squirrel monkeys after long-term monocular deprivation
K.-P. Hoffmann, C. Distler & O. J. Grüsser
European Journal of Neuroscience, 10:1136-1144, 1998
- Horizontal optokinetic nystagmus (OKN) as well as neuronal response properties in the nucleus of the optic
tract and the dorsal terminal nucleus of the accessory optic system (NOT-DTN) were investigated in three monocularly
deprived squirrel monkeys. In two monkeys occlusion of one eye was performed at birth (early) and in the third
after 7 weeks (late). In adulthood, in early deprived monkeys monocular horizontal OKN tested through the non-deprived
eye was symmetrical and in no way different from normal, i.e. stimulation in the temporonasal and nasotemporal
direction elicited equal and robust responses. OKN through the early occluded eye, however, was grossly abnormal
with low gain and great variability in the consistency of nasotemporal and temporonasal slow phase eye movements.
When in the late deprived monkey the non-deprived eye was occluded a strong spontaneous nystagmus developed despite
the deprived eye viewing a stationary pattern. The slow phases were directed from nasal to temporal for the deprived
eye. When tested through the non-deprived eye all neuronal responses of the NOT-DTN were normal. The deprived eye's
influence on NOT-DTN neurons was extremely weak. No neuron with a moderate or even dominant input from the deprived
eye was found after early deprivation. In the late deprived case the deficit was not as severe but still the non-deprived
eye was clearly dominating the responses in all neurons tested. Velocity tuning of neurons tested through the non-deprived
eye was normal and qualitatively corresponded well to slow phase eye velocity in response to equivalent retinal
slip during OKN. Through the early deprived eye, however, velocity tuning was extremely poor. It was somewhat better
through the late deprived eye. We suggest that the dramatic deterioration in the optokinetic reflex found after
long-term monocular deprivation for the amblyopic eye is probably caused by the almost complete loss of retinal
and cortical input driven by that eye to the NOT-DTN. These results are discussed in relation to our previous results
in cats and reports in the literature for humans with occlusion amblyopia.
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