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M. Marco–Gomariz, A. García–Avilés, L. Coll, R.D. Lund, M. Vidal–Sanz, M.P. Villegas–Pérez; Phototoxic Retinal Degeneration Causes Retinal Ganglion Cell Axonal Compression by Retinal Vessels . Invest. Ophthalmol. Vis. Sci. 2005;46(13):5235.
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Purpose: To study the chronology and topography of phototoxic retinal degeneration in order to compare it with the inherited retinal photoreceptor degeneration. Methods: The left pupil of Lister–Hooded and pigmented non–dystrophic Royal College of Surgeons (RCS) rats was dilated with atropine and the animals were exposed to light (3000 luxes) for 72 hours. Animals were processed between 0 and 365 days after light exposure. Before processing, the eye fundus was inspected and in some animals, type I horseradish peroxidase (HRP) or fluorescein isothiocyanate dextran (FID) was injected into the femoral vein to label the retinal vessels or Fluoro–Gold was applied to the superior colliculi to label retinal ganglion cells (RGCs). Retinas were dissected as whole mounts or processed for cross–sections, reacted for HRP demonstration or incubated with different antibodies (RT97, GFAP). Results: Both L–H and non–dystrophic RCS rats presented, immediately after light exposure, a distinct arciform area of retinal degeneration in the superotemporal retina that showed HRP and FID leakage and retinal pigment epithelial (RPE) cell migration towards more internal retinal layers. Although severe photorreceptor degeneration was observed all throughout the central retina, it was more severe in the superior retina and mainly in the arciform superotemporal area. Later, complexes formed by retinal venules surrounded by RPE cells showing HRP leakage developed in this more affected area and extended to the central retina. These vascular–RPE complexes were situated adjacent to Bruch's membrane and tractioned the inner retinal vessels, which in turn compressed the retinal ganglion cell (RGC) axons. Thus, axonal compression was seen in the areas where the vascular–RPE complexes developed. Conclusions: Phototoxic injury to the retina causes severe photoreceptor degeneration in the central retina that is most pronounced in an arciform region of the superotemporal retina. This is followed by RPE cell migration and development of RPE–vascular complexes nesxt to Bruch's membrane that traction the inner retinal vessels thus causing RGC axonal compression. These events have also been observed in dystrophic RCS rats and may thererefore be secondary to all forms of photoreceptor degeneration.
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