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Title 

Nox4-dependent H2O2 production contributes to chronic glutamate toxicity in primary cortical neurons

Authors 

Jong Seong HaJ E LeeJae-Ran LeeC S LeeJ S MaengY S BaeKi Sun KwonSung Sup Park

Publisher 

Elsevier

Issue Date 

2010

Citation 

Experimental Cell Research, vol. 316, no. 10, pp. 1651-1661

Keywords 

Chronic exposureGlutamate toxicityH2O2Nox4Reactive oxygen species

Abstract 

Reactive oxygen species (ROS) can trigger neuronal cell death and has been implicated in a variety of neurodegenerative diseases as well as brain ischemia. Here, we demonstrate that chronic (but not acute) glutamate toxicity in primary cortical neuronal cultures is associated with hydrogen peroxide (H2O2) accumulation in the culture medium and that neurotoxicity can be eliminated by external catalase treatment. Neuronal cultures in Ca2+-free medium or treated with BAPTA showed reduced glutamate-induced H2O2 generation, indicating that H2O2 generation is Ca2+-dependent. Pharmacological and genetic approaches revealed that NADPH oxidase plays a role in glutamate-induced H2O2 generation and that activation of NMDA and AMPA receptors is involved in this H2O2 generation. The Nox4 siRNA reduced NMDA-induced H2O2 production by 54% and cytotoxicity in parallel, suggesting that Nox4-containing NADPH oxidase functions NMDA receptor-mediated H2O2 production resulting in neurotoxicity. These findings suggest that the modulation of NADPH oxidase can be used as a new therapeutic strategy for glutamate-induced neuronal diseases.

ISSN 

0014-4827

Link 

http://dx.doi.org/10.1016/j.yexcr.2010.03.021

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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