Expression of glial fibrillary acidic protein (GFAP), glutamine synthetase (GS), and Bcl-2 protooncogene protein by Müller (glial) cells in retinal light damage of rats
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Abstract
In retinal light damage, degeneration of photoreceptors may cause alterations of glial
(Müller) cells. We performed immunocytochemical studies on Müller cells isolated from
retinae of rats exposed to enhanced illumination for 24 months, a procedure which
leads to complete loss of photoreceptor cells. One group of rats was fed daily with
Ginkgo biloba extract (EGb 761, an established free radical-scavenger) during the
last 8 months of life when the remaining photoreceptors (about 50%) die. We found
that (1) Müller cells respond to photoreceptor damage by increased expression of glial
fibrillary acidic protein, (2) Müller cells reduce expression of glutamine synthetase
when the major glutamate-releasing neurons are lost, and (3) the application of exogenous
free radical scavengers prevents the expression by Müller cells of the protooncogene
protein Bcl-2, a molecule assumed to activate endogenous free radical-scavenging activities.