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Daniel M. Albert, Richard R. Dubielzig, Travis D. Strong, Christine M. Sorenson, Nader Sheibani, David A. Lewis; Chronic Retinal Degeneration And Neovascular Proliferation In A Phototoxic Rat Model. Invest. Ophthalmol. Vis. Sci. 2011;52(14):976.
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© ARVO (1962-2015); The Authors (2016-present)
To document the chronic retinal degenerative changes in a phototoxic retinal degeneration, other than photoreceptor necrosis and loss, in the albino rat.
Light-induced changes were studied in 3-month old albino and pigmented rats following exposure to 12 hours of 3000 lux of cyclic light for periods ranging from 1-month to 9-months. Eyes of treated and control animals were studied by light microscopy and transmission electron microscopy. Research was conducted in compliance with the "ARVO Statement for the Use of Animals in Ophthalmic and Visual Sciences Research".
Phototoxic retinal degeneration was not produced in pigmented rats. After one-month exposure to cyclic light only necrotic or degenerative fragments of photoreceptor cells are still found. There are neovascular sprouts extending towards, but not yet entering, the RPE layer. The apeces of the RPE cells is thickened due to compact membranous change interpreted as smooth endoplasmic reticulum. By 3-months of exposure there is neovascular proliferation from the inner retina that displaces RPE multifocally. RPE cells sheath these vascular structures as they extend from the inner retina. No defects were seen in Bruch’s membrane at any stage of the disease studied. The abnormally distributed vessels have tight junctions supporting the hypothesis that they are derived from retinal and not choroidal vessels. This process is advanced to the same degree in animals exposed to light for one-month with a 5-month recovery as it is in animals exposed to light the entire 6-months.
Retinal degeneration, including neovascular proliferation occurs in albino rats with prolonged exposure to cyclic light. This degeneration leads to expected photoreceptor necrosis and loss early and to RPE remodeling and invasion of the RPE layer by neovascular proliferation of inner retinal vessels.
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