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Rearrangement of the cone mosaic in the retina of the rat model of retinitis pigmentosa

Authors

  • Yerina Ji,

    1. Neuroscience Graduate Program, University of Southern California, Los Angeles, California 90089-1111
    2. Center for Vision Science and Technology, University of Southern California, Los Angeles, California 90089-1111
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  • Colleen L. Zhu,

    1. Department of Biomedical Engineering, University of Southern California, Los Angeles, California 90089-1111
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  • Norberto M. Grzywacz,

    1. Neuroscience Graduate Program, University of Southern California, Los Angeles, California 90089-1111
    2. Center for Vision Science and Technology, University of Southern California, Los Angeles, California 90089-1111
    3. Department of Biomedical Engineering, University of Southern California, Los Angeles, California 90089-1111
    4. Department of Electrical Engineering, University of Southern California, Los Angeles, California 90089-1111
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  • Eun-Jin Lee

    Corresponding author
    1. Center for Vision Science and Technology, University of Southern California, Los Angeles, California 90089-1111
    2. Department of Biomedical Engineering, University of Southern California, Los Angeles, California 90089-1111
    • Department of Biomedical Engineering, Denney Research Building 140, Los Angeles, CA 90089-1111
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Abstract

In retinitis pigmentosa (RP), the death of cones normally follows some time after the degeneration of rods. Recently, surviving cones in RP have been studied and reported in detail. These cones undergo extensive remodeling in their morphology. Here we report an extension of the remodeling study to consider possible modifications of spatial-distribution patterns. For this purpose we used S334ter-line-3 transgenic rats, a transgenic model developed to express a rhodopsin mutation causing RP. In this study, retinas were collected at postnatal (P) days P5–30, 90, 180, and P600. We then immunostained the retinas to examine the morphology and distribution of cones and to quantify the total cone numbers. Our results indicate that cones undergo extensive changes in their spatial distribution to give rise to a mosaic comprising an orderly array of rings. These rings first begin to appear at P15 at random regions of the retina and become ubiquitous throughout the entire tissue by P90. Such distribution pattern loses its clarity by P180 and mostly disappears at P600, at which time the cones are almost all dead. In contrast, the numbers of cones in RP and normal conditions do not show significant differences at stages as late as P180. Therefore, rings do not form by cell death at their centers, but by cone migration. We discuss its possible mechanisms and suggest a role for hot spots of rod death and the remodeling of Müller cell process into zones of low density of photoreceptors. J. Comp. Neurol., 2012. © 2011 Wiley Periodicals, Inc.

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