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Exp Neurobiol 2005; 14(1): 29-40
Published online November 30, -0001
© The Korean Society for Brain and Neural Sciences
Sun-Hwa Park, Su-Ja Oh*, Jun-Won Park, Sung-Jin Park, Jin-Woong Chung and Myung-Hoon Chun
Department of Anatomy, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea
Correspondence to: *To whom correspondence should be addressed.
TEL: 82-2-590-1155, FAX: 82-2-536-3110
Excitotoxicity in the retina may result from abnormality of glutamate turnover mechanisms. Glutamate turnover in the retina is mainly managed by Müller cells. The present study thus has been investigated the correlation between alteration of glutamate turnover mechanisms and the glial reactions in retinal Müller cells, and their survival in experimental insulin-dependent diabetes to improve protective mechanisms against diabetic retinopathy. Rats were intravenously injected with streptozotocin. Animals with blood glucose levels over 300 mg/dl were classified as diabetic and housed for 1, 4, 12, or 24 weeks. The retinas were processed for immunochemical analysis using anti-GLAST, anti-glutamine synthetase (GS), anti-vimentin, anti-GFAP, and anti-PCNA antibodies. In normal retinas, GLAST and GS were localized in Müller cells, the outer plexiform layer, the border between the inner nuclear layer and the inner plexiform layer, and in a band in the middle of the inner plexiform layer. Decrease of both GLAST and GS reactivity was prominent in the outer plexiform layer after 12 weeks diabetes. GS levels throughout the diabetic periods gradually dropped. Vimentin was localized in the radial processes, and GFAP in some end feet of Müller cells at normal. GFAP level at 12 weeks and 24 weeks diabetes was four and six folds higher than at normal, with increased labeling in the radial processes of Müller cells. Most Müller cells showed PCNA labeling by 12 weeks diabetes. These results suggest that up-regulated GFAP in the diabetic Müller cells may play a self protective role for excitotoxic condition produced by downregulated GS and GLAST.
Keywords: glutamate transporter, glutamine synthetase, retina, glial reaction, immunohistochemistry, diabetes, rat