September 1995
Volume 36, Issue 10
Free
Articles  |   September 1995
Protective action of zinc against glutamate neurotoxicity in cultured retinal neurons.
Author Affiliations
  • M Kikuchi
    Department of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.
  • S Kashii
    Department of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.
  • Y Honda
    Department of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.
  • H Ujihara
    Department of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.
  • M Sasa
    Department of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.
  • Y Tamura
    Department of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.
  • A Akaike
    Department of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.
Investigative Ophthalmology & Visual Science September 1995, Vol.36, 2048-2053. doi:
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    • Get Citation

      M Kikuchi, S Kashii, Y Honda, H Ujihara, M Sasa, Y Tamura, A Akaike; Protective action of zinc against glutamate neurotoxicity in cultured retinal neurons.. Invest. Ophthalmol. Vis. Sci. 1995;36(10):2048-2053.

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

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Abstract

PURPOSE: To examine the effects of Zn2+ on glutamate-induced neurotoxicity in cultured retinal neurons. METHODS: Primary cultures obtained from fetal rat retinas (16 to 19 days gestation) were used. The neurotoxic effects of excitatory amino acids were quantitatively assessed using the trypan blue exclusion method. RESULTS: A brief exposure of retinal cultures to glutamate or N-methyl-D-aspartate (NMDA) induced delayed cell death. Zn2+ at concentrations of 3 to 30 microM ameliorated glutamate- and NMDA-induced neurotoxicity in a dose-dependent manner. By contrast, neurotoxicity induced by a 1-hour exposure to kainate was not affected by Zn2+. CONCLUSIONS: These findings demonstrate that Zn2+ protects retinal neurons from NMDA receptor-mediated glutamate neurotoxicity.

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