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Abstract
Glial fibrillary acidic protein (GFAP) is normally found in astrocytes. In the normal rat retina at all ages, only astrocytes stain for GFAP. This staining pattern is also found in RCS rats with inherited retinal dystrophy younger than 38 days. Beginning on day 38, when about 61% of the photoreceptors have degenerated, a few GFAP-positive fibers span the retina from the inner limiting membrane to the external limiting membrane. By day 41 and at all later ages examined, the radial fibers of Müller cells is a response to photoreceptor necrosis or might be a direct effect of the mutant gene, we induced photoreceptor degeneration in normal, adult Sprague-Dawley rats by exposing them to constant light for variable periods of time. After 3 days in constant light, there is a 20% reduction in the number of photoreceptors and many Müller cells are positive for GFAP. Immunoblot studies confirmed that the anti-GFAP reacted with a single protein from retina that corresponded in molecular weight and Triton-insolubility to GFAP. The immunoblots also corroborated the results from anti-GFAP immunostaining of control and experimental retinas. These results indicate that Müller cells express GFAP immunoreactivity in response to experimentally as well as genetically induced photoreceptor degeneration.