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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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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.
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