May 2005
Volume 46, Issue 13
ARVO Annual Meeting Abstract  |   May 2005
Rod Development in a Mutant Mouse With Diminished Cones
Author Affiliations & Notes
  • R.E. Karcavich
    Biology and Center for Regenerative Biology and Medicine, IUPUI, Indianapolis, IN
  • C. Scott
    Biology and Center for Regenerative Biology and Medicine, IUPUI, Indianapolis, IN
  • S.–L. Fong
    Ophthalmology, Indiana University, Indianapolis, IN
  • W.–B. Fong
    Ophthalmology, Indiana University, Indianapolis, IN
  • T. Belecky–Adams
    Biology and Center for Regenerative Biology and Medicine, IUPUI, Indianapolis, IN
  • Footnotes
    Commercial Relationships  R.E. Karcavich, None; C. Scott, None; S. Fong, None; W. Fong, None; T. Belecky–Adams, None.
  • Footnotes
    Support  NEI fellowship EYO6642, March of Dimes, Research to Prevent Blindness, Knights Templar Eye Fdn, Inc
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 3977. doi:
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      R.E. Karcavich, C. Scott, S.–L. Fong, W.–B. Fong, T. Belecky–Adams; Rod Development in a Mutant Mouse With Diminished Cones . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3977.

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

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Abstract: : Purpose: Previous results using a transgenic mouse line in which majority of cone photoreceptors have been ablated by expressing diphtheria toxin under control of a cone specific promoter showed a loss of cones early in optic cup development followed by a loss of ventral rods during postnatal retinal development. The goal of this study was to determine whether cone cell loss leads to subsequent degeneration or a fate change of the rods. Methods: Sections through the eyes of heterozygous transgenic and non–transgenic littermates were examined at postnatal stages (P0–P9) using immunohistochemical and in situ hybridization to determine cell type specific expression patterns and potential changes in mitosis or cell death. Results:At all developmental stages examined, the differentiation of rods in the dorsal hemi–retinae of non–transgenic and transgenic littermates were similar in numbers, expression level and expression patterns. Cells expressing photoreceptor–specific markers are found next to the ventricular layer in the region that will give rise to the outer nuclear layer in both transgenic and non–transgenic littermates. Until P3, the development of photoreceptors in the ventral hemi–retinae of transgenic and non–transgenic littermates is indistinguishable, but by P3, both the number and expression level of markers in the presumptive photoreceptors was drastically reduced in the ventral portion of the transgenic mice. Examination of pyknotic nuclei in hematoxylin and eosin stained sections through transgenic and non–transgenic mice showed no detectable differences. Ongoing studies are focused on investigating potential changes in mitosis, cell death, and cell type–specific expression patterns in these mice. Conclusions: 1) Cone photoreceptors appear to affect the survival and/or differentiation of rod photoreceptors during development of the retina, and 2) this transgenic mouse line is a suitable model for studying interactions between photoreceptor subtypes and diseases involving photoreceptor loss. .

Keywords: photoreceptors • retinal development • transgenics/knock-outs 

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