April 1997
Volume 38, Issue 5
Free
Articles  |   April 1997
Protective effects of methylcobalamin, a vitamin B12 analog, against glutamate-induced neurotoxicity in retinal cell culture.
Author Affiliations
  • M Kikuchi
    Department of Ophthalmology, Graduate School of Medicine, Faculty of Pharmaceutical Sciences, Kyoto University, Japan.
  • S Kashii
    Department of Ophthalmology, Graduate School of Medicine, Faculty of Pharmaceutical Sciences, Kyoto University, Japan.
  • Y Honda
    Department of Ophthalmology, Graduate School of Medicine, Faculty of Pharmaceutical Sciences, Kyoto University, Japan.
  • Y Tamura
    Department of Ophthalmology, Graduate School of Medicine, Faculty of Pharmaceutical Sciences, Kyoto University, Japan.
  • K Kaneda
    Department of Ophthalmology, Graduate School of Medicine, Faculty of Pharmaceutical Sciences, Kyoto University, Japan.
  • A Akaike
    Department of Ophthalmology, Graduate School of Medicine, Faculty of Pharmaceutical Sciences, Kyoto University, Japan.
Investigative Ophthalmology & Visual Science April 1997, Vol.38, 848-854. doi:
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      M Kikuchi, S Kashii, Y Honda, Y Tamura, K Kaneda, A Akaike; Protective effects of methylcobalamin, a vitamin B12 analog, against glutamate-induced neurotoxicity in retinal cell culture.. Invest. Ophthalmol. Vis. Sci. 1997;38(5):848-854.

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

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Abstract

PURPOSE: To examine the effects of methylcobalamin on glutamate-induced neurotoxicity in the cultured retinal neurons. METHODS: Primary cultures obtained from the fetal rat retina (gestation days 16 to 19) were used for the experiment. The neurotoxicity was assessed quantitatively using the trypan blue exclusion method. RESULTS: Glutamate neurotoxicity was prevented by chronic exposure to methylcobalamin and S-adenosylmethionine (SAM), which is formed in the metabolic pathway of methylcobalamin. Chronic exposure to methylcobalamin and SAM also inhibited the neurotoxicity induced by sodium nitroprusside that release nitric oxide. By contrast, acute exposure to methylcobalamin did not protect retinal neurons against glutamate neurotoxicity. CONCLUSIONS: Chronic administration of methylcobalamin protects cultured retinal neurons against N-methyl-D-aspartate-receptor-mediated glutamate neurotoxicity, probably by altering the membrane properties through SAM-mediated methylation.

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