May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
A Gene Responsible for Light-induced Visual Impairment (lvi) in Mice
Author Affiliations & Notes
  • B. Chang
    The Jackson Laboratory, Bar Harbor, ME, United States
  • N.L. Hawes
    The Jackson Laboratory, Bar Harbor, ME, United States
  • R.E. Hurd
    The Jackson Laboratory, Bar Harbor, ME, United States
  • R.L. Miller
    Alma College, Alma, MI, United States
  • M.T. Davisson
    Alma College, Alma, MI, United States
  • S. Nusinowitz
    Harbor-UCLA Medical Center, Jules Stein Eye Institute, Torrance, CA, United States
  • J.R. Heckenlively
    Harbor-UCLA Medical Center, Jules Stein Eye Institute, Torrance, CA, United States
  • Footnotes
    Commercial Relationships  B. Chang, None; N.L. Hawes, None; R.E. Hurd, None; R.L. Miller, None; M.T. Davisson, None; S. Nusinowitz, None; J.R. Heckenlively, None.
  • Footnotes
    Support  NIH Grant EY07758
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 4532. doi:
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      B. Chang, N.L. Hawes, R.E. Hurd, R.L. Miller, M.T. Davisson, S. Nusinowitz, J.R. Heckenlively; A Gene Responsible for Light-induced Visual Impairment (lvi) in Mice . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4532.

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

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Abstract

Abstract: : Purpose: Visual impairment by environmental factors such as light overexposure is preventable if the susceptibility factors or genes can be identified. Here we report a gene responsible for light-induced visual impairment (lvi) in mice, its chromosomal localization and the clinical appearance and histology of light-treated susceptible mice. Methods: While screening mouse strains for light sensitivity, we discovered a mutation that causes light induced non-photoreceptor related damage. To map lvi, homozygous mutant mice were bred to normal mice and the mice of the F2 generation were exposed to constant light at 1200 ft-c for nine days. Following exposure, we characterized the clinical effects of this new gene responsible for light-induced visual impairment using electroretinography (ERG) and histology and performed a genome scan of DNA markers. Results: Untreated mice homozygous for the lvi mutation have a normal ERG response and a normal histology; however, after 9 days of light treatment, the ERG responses showed a much reduced or no b-wave in dark-adapted ERG and the amplitude of the cone ERG was drastically reduced. The histology showed a very thin or missing outer plexiform layer (OPL) in the retina. Genetic analysis showed that lvi is an autosomal recessive mutation and maps to mouse Chromosome 18. Conclusions: The OPL damage induced by light overexposure is a novel finding. The visual impairment might be caused by OPL damage in mice homozygous for the lvi mutation because the normal transmission between photoreceptors and bipolar cells is dependent on a normal OPL. The phenotype of the mice with lvi mutation after light overexposure is similar to human patients with incomplete congenital stationary night blindness (CSNB2) and it provides a mouse model to study the mechanism related to this type of disease in human.

Keywords: gene mapping • animal model • retina 
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