December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Paucity Of Horizontal Connections For Binocular Vision Within Primary Visual Cortex Of Naturally-strabismic Macaque
Author Affiliations & Notes
  • L Tychsen
    Ophthalmology and Visual Sciences Washington Uiversity School of Medicine St Louis MO
  • A Burkhalter
    Neurobiology and Anatomy
    Washington Uiversity School of Medicine St Louis MO
  • AM F Wong
    Ophthalmology and Visual Sciences
    Washington Uiversity School of Medicine St Louis MO
  • Footnotes
    Commercial Relationships   L. Tychsen, None; A. Burkhalter, None; A.M.F. Wong, None. Grant Identification: Support: NIH Grant EY10214
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 2623. doi:
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      L Tychsen, A Burkhalter, AM F Wong; Paucity Of Horizontal Connections For Binocular Vision Within Primary Visual Cortex Of Naturally-strabismic Macaque . Invest. Ophthalmol. Vis. Sci. 2002;43(13):2623.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: To determine the structural basis for visuomotor deficits in infantile esotropia, we investigated intrinsic horizontal connections in the primary visual cortex (striate cortex, area V1) of three strabismic adult macaque monkeys. Methods: Each animal was documented to have onset of natural esotropia (the visual axes deviated nasally) in early infancy. Behavioral testing showed normal visual acuity in both eyes, and ocular motor deficits mimicking those of humans who have early-onset strabismus. Three adult macaques with normal eye alignment served as controls. To label horizontal connections, the neuronal tracer biotinylated-dextran-amine (BDA) was injected at multiple locations across opercular area V1. After a short survival time the animals were perfused and area V1 was flattened and sectioned tangential to the pial surface. Connections between right eye and left eye ocular dominance columns were analyzed by overlaying BDA-stained sections with adjacent sections stained to reveal cytochrome oxidase (CO). Results: Binocular connections in strabismic animals' cortex were reduced 50-60% compared to normal monkey, with the greatest reduction occurring in animals who had marked ocular motor deficits. In strabismic monkeys, labeled patches of horizontal axonal projections terminated significantly more frequently in same-eye (69-77%) as opposed to opposite-eye (24-31%) ocular dominance columns (ODCs). Counts of synaptic boutons in same-eye ODCs exceeded those in opposite-eye ODCs by 53-60%. The quantitative deficiency in binocular connections was obvious qualitatively as a consistent "skip" pattern in labeling of neuronal projections. The paucity of binocular connections was similar for neurons residing in CO-interblob and blob compartments of layers 2/3 and 4B. Conclusion: Maldevelopment of binocular connections is a consistent finding in primates who exhibit the visuomotor deficits that characterize human infantile strabismus. Monkeys with severe behavioral deficits have the most striking V1 abnormalities.

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