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• W1979026156 abstract "Previously, we showed that dopamine protects cultured retinal neurons from N-methyl-D-aspartate (NMDA) receptor mediated-glutamate excitotoxicity via dopamine D1 receptor. This study has demonstrated for the first time that nitric oxide synthase (NOS) plays a crucial role in dopamine-induced neuroprotection. Our patch clamp study has shown that dopamine does not affect the NMDA-induced whole cell current. Dopamine or SKF38393 (D1 receptor agonist) inhibited ionomycin (calcium ionophore)-induced toxicity, while dopamine did not affect S-nitrosocysteine (NO donor)-induced toxicity. Biochemical analysis on enzymatic activities has shown that dopamine or cAMP (which is generated through D1 receptor stimulation) inhibits glutamate induced-NOS activation. These results suggest that dopamine inhibits glutamate induced-NOS activation via D1 receptor, resulting in the protection of retinal neurons." @default.
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• W1979026156 date "2003-08-01" @default.
• W1979026156 modified "2023-09-25" @default.
• W1979026156 title "Inhibition of glutamate-induced nitric oxide synthase activation by dopamine in cultured rat retinal neurons" @default.
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• W1979026156 doi "https://doi.org/10.1016/s0304-3940(03)00669-4" @default.
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