September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Neural Mechanisms for Binocular Oculomotor Signaling in Strabismus
Author Affiliations & Notes
  • Michael J. Mustari
    University of Washington, Seattle, Washington, United States
  • Footnotes
    Commercial Relationships   Michael Mustari, None
  • Footnotes
    Support  EY06069; EY024848; ORIP P51 OD010425
Investigative Ophthalmology & Visual Science September 2016, Vol.57, No Pagination Specified. doi:
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      Michael J. Mustari; Neural Mechanisms for Binocular Oculomotor Signaling in Strabismus. Invest. Ophthalmol. Vis. Sci. 201657(12):.

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      © 2017 Association for Research in Vision and Ophthalmology.

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Abstract

Presentation Description : High acuity vision in primates depends on the fovea of each eye. The oculomotor system controls eye alignment and movement so that the foveae are directed at an object of interest. Full visual function in primates requires coordinated binocular experience in early life. If this experience is disrupted, permanent loss of normal eye alignment (strabismus) and deficits in visual function (amblyopia) can occur. Improving treatment for various forms of strabismus requires understanding neural mechanisms for binocular oculomotor control.
Human and nonhuman primates have similar visual and oculomotor systems, and dependence on early visual experience. Establishment of nonhuman primate models for developmental strabismus facilitates discovery of neural mechanisms for normal and strabismic eye alignment and eye movements. Recent studies have discovered a loss of normal binocular visual sensitivity in primary visual cortex and extrastriate visual areas (MT, MST) that could lead to visual suppression and alterations in the calibration of distal oculomotor centers. For example, horizontal medial rectus and vertical lateral rectus motoneurons have been shown to encode

cross-axis smooth pursuit movements in pattern strabismus. Recently, we found abnormalities in the paramedian pontine reticular formation (PPRF), which carries signals related to instantaneous, horizontal saccadic velocity. Microstimulation (MS) of the PPRF of normal animals evokes conjugate horizontal ramp eye movements. In contrast, MS of PPRF of strabismic animals evokes disconjugate movements with each eye moving at different velocities and in different directions. Neurons in PPRF of these animals showed an abnormally broad distribution of preferred directions and 12/60 even preferring vertical saccades. These findings suggest that a neural mechanism, acting alone, could explain disconjugacies in some forms of strabismus. This does not rule out abnormalities in orbital tissues, eye muscle pulleys, or eye muscles themselves in different forms of strabismus.
Taken together, these studies suggest that interference with coordinated binocular visual-oculomotor experience during an early sensitive period disrupts the calibration and normal tuning of brain areas from visual cortex reaching to ocular motoneurons that are essential for maintaining eye alignment and eye movements.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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