February 1994
Volume 35, Issue 2
Free
Articles  |   February 1994
Protective action of dopamine against glutamate neurotoxicity in the retina.
Author Affiliations
  • S Kashii
    Department of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.
  • M Takahashi
    Department of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.
  • M Mandai
    Department of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.
  • H Shimizu
    Department of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.
  • Y Honda
    Department of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.
  • M Sasa
    Department of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.
  • H Ujihara
    Department of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.
  • Y Tamura
    Department of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.
  • T Yokota
    Department of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.
  • A Akaike
    Department of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.
Investigative Ophthalmology & Visual Science February 1994, Vol.35, 685-695. doi:
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      S Kashii, M Takahashi, M Mandai, H Shimizu, Y Honda, M Sasa, H Ujihara, Y Tamura, T Yokota, A Akaike; Protective action of dopamine against glutamate neurotoxicity in the retina.. Invest. Ophthalmol. Vis. Sci. 1994;35(2):685-695.

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

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Abstract

PURPOSE: The electrophysiologic study using patch-clamp techniques demonstrated that NMDA-induced currents had properties similar to those recorded in the brain. METHODS: Primary cultures obtained from the fetal rat retina (gestation days 16 to 19) were used for the experiment. Immunocytochemical and electrophysiologic studies were done to identify the cultured cells. The neurotoxic effects of glutamate or N-methyl-D-aspartate (NMDA) on the retinal cultures were quantitatively assessed using the trypan blue exclusion method. RESULTS: The immunocytochemical study revealed that the major component of the rat retinal cultures was neurons including amacrine cells. The electrophysiologic study using patch-clamp techniques demonstrated that exposure to NMDA-induced currents with properties characteristic of those recorded in the brain. Brief exposure of these neurons to glutamate or NMDA induced delayed cell death. Glutamate neurotoxicity was prevented by the application of dopamine and forskolin. The protective action of dopamine was antagonized by a D1 receptor antagonist (SCH 23390) but not by D2 receptor antagonists (domperidone and sulpiride). A D1 receptor agonist (SKF 38393) protected glutamate-induced neurotoxicity in a concentration-dependent manner, whereas a D2 receptor agonist (quinpirole) did not affect it. CONCLUSIONS: These findings demonstrate that dopamine protects retinal neuronal cells against NMDA receptor-mediated glutamate neurotoxicity via D1 receptors.

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