Abstract
Abstract: :
Purpose: To study the chronology and topography of phototoxic retinal degeneration. Methods: The left pupil of Lister–Hooded and pigmented non–dystrophic RCS rats was dilated with atropine and the animals were exposed to light (3000 luxes) for 72 hours. Animals were processed 0, 7, 30, 90 and 180 days after light exposure. Before processing, the eye fundus was inspected and type I horseradish peroxidase (HRP) was injected in the femoral vein. The retinas were dissected as whole mounts or processed for cross–sections, reacted for HRP demonstration and incubated with the RT 97 antibody (against the 200 kd neurofilament subunit). Results: Both L–H and non–dystrophic RCS rats presented, immediately after light exposure, a distinct area of retinal degeneration in the left superotemporal retina. This area had an oval shape and formed an arc around the optic disc. Its largest diameter varied between 3.5 and 6.5 mm and its proximal border was located at a distance of 1to 2 mm from the optic disc. Within this lesioned area, the most affected layers were the outer retinal layers, where the pigment epithelial cells migrated to the outer vascular plexus, this plexus becoming thinner and disappearing with time. Three months or more after light exposure, the retinas showed a second pathologic event: the outer vascular plexus also became affected in the central retina. Conclusions: Phototoxic injury to the retina produces in LH and non–dystrophic RCS rats at least two separate pathologic events: an early arciform area of retinal degeneration in the superotemporal retina and a delayed degeneration in the central retina.
Keywords: retinal degenerations: cell biology • photoreceptors • retinal degenerations: hereditary