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Tat-NR2B9c Prevents Excitotoxic Neuronal Superoxide Production
Author(s) -
Yanting Chen,
Angela M. BrennanMinnella,
Sunil A. Sheth,
Jamel ElBenna,
Raymond A. Swanson
Publication year - 2015
Publication title -
journal of cerebral blood flow and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.167
H-Index - 193
eISSN - 1559-7016
pISSN - 0271-678X
DOI - 10.1038/jcbfm.2015.16
Subject(s) - neuroprotection , nmda receptor , superoxide , nadph oxidase , nitric oxide , postsynaptic potential , chemistry , receptor , glutamate receptor , pharmacology , excitotoxicity , neuroscience , microbiology and biotechnology , biochemistry , biology , reactive oxygen species , enzyme , organic chemistry
The Tat-NR2B9c peptide has shown clinical efficacy as a neuroprotective agent in acute stroke. Tat-NR2B9c is designed to prevent nitric oxide (NO) production by preventing postsynaptic density protein 95 (PSD-95) binding to N-methyl-D-aspartate (NMDA) receptors and neuronal nitric oxide synthase; however, PSD-95 is a scaffolding protein that also couples NMDA receptors to other downstream effects. Here, using neuronal cultures, we show that Tat-NR2B9c also prevents NMDA-induced activation of neuronal NADPH oxidase, thereby blocking superoxide production. Given that both superoxide and NO are required for excitotoxic injury, the neuroprotective effect of Tat-NR2B9c may alternatively be attributable to uncoupling neuronal NADPH oxidase from NMDA receptor activation.

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