May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Protective Effects of Selegiline Against Glutamate Neurotoxicity in Cultured Retinal Neurons
Author Affiliations & Notes
  • S. Kashii
    Department of Ophthalmology, Osaka Red Cross Hospital, Osaka, Japan
    Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan
  • T. Yamauchi
    Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan
  • K. Takahata
    Institute of Research and Development, Osaka, Japan
  • S. Muraoka
    Institute of Research and Development, Osaka, Japan
  • F. Yoneda
    Institute of Research and Development, Osaka, Japan
  • A. Akaike
    Pharmacology, Kyoto University Graduate School of Pharmaceutical Sciences, Kyoto, Japan
  • Footnotes
    Commercial Relationships  S. Kashii, None; T. Yamauchi, None; K. Takahata, Fujimoto Pharmaceutical Corporation E; S. Muraoka, Fujimoto Pharmaceutical Corporation E; F. Yoneda, Fujimoto Pharmaceutical Corporation E; A. Akaike, None.
  • Footnotes
    Support  Grant–in–Aid 13470366 and 14370780
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 3263. doi:
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      S. Kashii, T. Yamauchi, K. Takahata, S. Muraoka, F. Yoneda, A. Akaike; Protective Effects of Selegiline Against Glutamate Neurotoxicity in Cultured Retinal Neurons . Invest. Ophthalmol. Vis. Sci. 2004;45(13):3263.

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

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Abstract

Abstract: : Purpose: To study the effect of selegiline, a selective monoamine oxidase–B inhibitor, and its metabolite, desmethylselegiline, on glutamate neurotoxicity in cultured retinal neurons. Methods: Primary cultures were obtained from fetal rat retinae (gestation day 17–19). Cytosine arabinoside (10 µM) was added to the culture on the 6th day to eliminate non–neuronal cells. We used only those cultures maintained for 7–8 days in vitro. Glutamate neurotoxicity was assessed by 10–min exposure to 1mM glutamate followed by 1–hour incubation in glutamate–free media, using the trypan blue exclusion method. Selegiline or desmethylselegiline were applied simultaneously with 1mM glutamate. Results: Ten–min exposure to glutamate followed by 1–hour incubation reduced cell viability by 20–40%. Simultaneous application of selegiline (1, 10, 100 µM) and glutamate (1mM) inhibited retinal neuronal cell death induced by glutamate in a dose–dependent manner. Cell viability was also restored by co–application of 10 µM desmethylselegiline, a selegiline metabolite, with glutamate (1mM) in a similar manner to that seen with selegiline (10 µM). Conclusions: These results suggest that selegiline or its desmethyl metabolite has a protective action against glutamate–induced neurotoxicity in cultured retinal neurons.

Keywords: excitatory amino acid receptors • retinal culture • cell death/apoptosis 
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