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Michael Mustari, Seiji Ono; Neural Mechanisms for smooth pursuit and vestibular ocular behavior in strabismic monkeys. Invest. Ophthalmol. Vis. Sci. 2013;54(15):1931.
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To examine a moving object in detail we use smooth pursuit (SP) eye movements to maintain its image on the fovea. The visual and oculomotor systems are immature at birth and require binocular visual-motor experience for calibration. At least 3% of children born in the U.S. have disorders of eye alignment (strabismus), impaired oculomotility, and gaze instability (e.g., latent nystagmus). Our studies address neural mechanisms for visual processing in the cerebral cortex for generation of SP.
We studied SP, ocular following (OFR) and vestibular ocular reflex (VOR) behavior in normal and esotropia (ET) monkeys (M. mulatta). Experimental strabismus was produced with either surgical or prism-goggle methods. Surgery (1-2 wks of age) involved resection of the medial rectus and recession of the lateral rectus muscles of one eye. Prism-goggle rearing (first 3 months of life) deviated the horizontal optic axis of the right eye and vertical optic axis of the left eye by 20 prism diopters. We studied the eye movements of ET and normal monkeys when they were at least 2 years of age using electromagnetic methods employing scleral search coils. Extracellular single unit recording was accomplished with metal microelectrodes and standard methods.
Both surgical and prism reared animals developed similar syndrome components including esotropia (10°-20°), latent nystagmus (<4°/s) and asymmetric SP (nasalward gains > temporalward). During visual-vestibular testing strabismic monkeys showed symmetric horizontal VORs in dark or light. In contrast, suppression of the VOR using a visual target that moved with the head was impaired. The VOR suppression deficit was consistent with the SP bias. The OFR showed significantly less asymmetry than SP. In single unit recording studies, we found that medial superior temporal cortex (MSTd and MSTl) neurons in our ET monkeys display a loss of binocular visual and SP sensitivity. This ocular bias may distributed to distal cortical (FEF) and brainstem targets (NOT, DLPN, NRTP), which play complimentary roles in SP, optokinesis and latent nystagmus.
Early disruption of binocular visual experience can lead to developmental strabismus with similar syndrome components in children and monkeys. Here we show that disorders of smooth pursuit are likely due to disruption of the cortical pursuit system and not distal motor sites involving VOR pathways.
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