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.
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.
Grosche
J
J
Carl Ludwig Institute of Physiology, Leipzig University, Germany.
Härtig
W
W
Reichenbach
A
A
D000818:Animals; D005904:Glial Fibrillary Acidic Protein / Q000235:genetics*; D005974:Glutamate-Ammonia Ligase / Q000235:genetics*; D007150:Immunohistochemistry; D008027:Light; D008297:Male; D009457:Neuroglia / Q000473:pathology*; D015513:Oncogene Proteins / Q000235:genetics*; D051381:Rats; D012160:Retina
D005904:Glial Fibrillary Acidic Protein; D015513:Oncogene Proteins; D005974:Glutamate-Ammonia Ligase