May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
The effect of glutamate excitotoxicity on the dopaminergic cells in the rat retina
Author Affiliations & Notes
  • S.J. Park
    Department of Anatomy, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea
  • E.–J. Lim
    Department of Anatomy, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea
  • S.–J. Oh
    Department of Anatomy, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea
  • M.–H. Chun
    Department of Anatomy, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea
  • Footnotes
    Commercial Relationships  S.J. Park, None; E. Lim, None; S. Oh, None; M. Chun, None.
  • Footnotes
    Support  none
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 3268. doi:
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      S.J. Park, E.–J. Lim, S.–J. Oh, M.–H. Chun; The effect of glutamate excitotoxicity on the dopaminergic cells in the rat retina . Invest. Ophthalmol. Vis. Sci. 2004;45(13):3268.

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

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Abstract

Abstract: : Purpose: To investigate the effect of glutamate excitotoxicity on the dopaminergic cells in the rat retina. Methods: L–glutamate (5mg/g) was subcutaneously injected to 9 days old rats. Rats were sacrificed at postnatal day 49. Vibratome sections (40 µm thick) and dissociated cells were double labeled using monoclonal or polyclonal TH (Chemicon 1:1000) antisera with following antibodies; monoclonal calbindin D–28k (Sigma 1:3000), polyclonal calretinin (Chemicon 1:1000), monoclonal NMDA receptor 1 (NR1) (Chemicon 1:1000), polyclonal glutamate receptor (GluR) 2/3 (Chemicon 1:1000) and monoclonal GluR6/7 (Chemicon 1:1000). We also examined the level of NR1 protein by western blot analysis in the normal and injected retinas. The cell density of TH immunoreactive cells was also examined. Results: The density of TH labeled cells was not changed compared with those of control retina. TH labeled cells expressed two kinds of calcium binding proteins, calbindin D–28k and calretinin. TH labeled cells also expressed GluR 2/3 (AMPA receptor) and GluR 6/7 (Kainate receptor) but not NR1 (NMDA receptor). NR1 protein level in the glutamate injected retinas decreased to 50% of the control level. Conclusions: The possible reasons of TH labeled cells resistant to glutamate toxicity may be due to the expression of calcium binding proteins (calbindin and calretinin) and the absence of NR1 in TH labeled cells.

Keywords: retinal degenerations: cell biology • amacrine cells • dopamine 
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