May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Inverse Correlation of Glutamate Turnover and Glial Reaction in Insulin-dependent Diabetic Rat Retinas - In Respect to GLAST and Glutamine Synthetase, and GFAP Immunoreactivity
Author Affiliations & Notes
  • S. Oh
    Department of Anatomy, Catholic University of Korea, Seoul, Republic of Korea
  • S. Park
    Department of Anatomy, Catholic University of Korea, Seoul, Republic of Korea
  • J. Park
    Department of Anatomy, Catholic University of Korea, Seoul, Republic of Korea
  • J. Chung
    Department of Anatomy, Catholic University of Korea, Seoul, Republic of Korea
  • M. Chun
    Department of Anatomy, Catholic University of Korea, Seoul, Republic of Korea
  • Footnotes
    Commercial Relationships  S. Oh, None; S. Park, None; J. Park, None; J. Chung, None; M. Chun, None.
  • Footnotes
    Support  Korea Health 21 R&D Project 01-PJ1-PG3-20700-0048
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 3882. doi:
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      S. Oh, S. Park, J. Park, J. Chung, M. Chun; Inverse Correlation of Glutamate Turnover and Glial Reaction in Insulin-dependent Diabetic Rat Retinas - In Respect to GLAST and Glutamine Synthetase, and GFAP Immunoreactivity . Invest. Ophthalmol. Vis. Sci. 2003;44(13):3882.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: The present study has been conducted to clarify the relationship of glutamate homeostasis and glial reaction in the rat retinal Muller cells depending on diabetic state, which was induced by a streptozotocin injection. Methods: Young adult male Sprague-Dawley rats were intravenously injected with streptozotocin (in 0.05M sodium citrate buffer, pH 5.5) at a dose of 60 mg/kg body weight. Animals over 300 mg/dl in blood glucose level were classified as diabetic and housed carefully for 1, 4, 12, and 24 weeks. At each time point, the retinas were dissected out and processed for immunohistochemical and immunoblotting analyses using by anti-L-glutamate/L-aspartate transporter (GLAST), anti-glutamine synthetase (GS), and anti-GFAP antibodies. Results: In the normal retina, GLAST and GS were immunolocalized in the Muller cells, the outer plexiform layer (OPL), the border between the inner nuclear layer and the inner plexiform layer (IPL), and a band in the middle of the IPL. The expression of both proteins was decreased remarkably in the OPL by 12 weeks of diabetes and increased slightly in the end feet of the Muller cells from 4 weeks onwards. Immunoblotting results of the two proteins in the diabetic retinas were largely consistent with those of immunohistochemistry. GFAP immunoreactivity in the end feet of the Muller cells appeared by 1week of diabetes, was dispersed into radial processes at 4 weeks and prominently increased at 12 and 24 weeks. Conclusions: These results suggest that glutamate turnover decreasing via down-regulated GLAST and GS and glial reaction representing by up-regulated GFAP are inversely reacted in the Muller cells on diabetic state.

Keywords: diabetes • retinal degenerations: cell biology • Muller cells 
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