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Superoxide generation via the NR2B-NMDAR/RasGRF1/NOX2 pathway promotes dendritogenesis

dc.contributor.authorAbarzúa S.
dc.contributor.authorAmpuero E.
dc.contributor.authorvan Zundert B.
dc.date.accessioned2020-09-02T22:11:05Z
dc.date.available2020-09-02T22:11:05Z
dc.date.issued2019
dc.identifier10.1002/jcp.28859
dc.identifier.citation234, 12, 22985-22995
dc.identifier.issn00219541
dc.identifier.urihttps://hdl.handle.net/20.500.12728/3515
dc.descriptionN-methyl-D-aspartate receptors (NMDARs) that contain the NR2A and NR2B subunits play a critical role in neuronal plasticity and dendritogenesis. Gain-and-loss-of function studies indicate that NR2B, but not NR2A, promotes dendritic branching. Accumulating evidence indicates that stimulation of NMDARs activates NADPH oxidase (NOX2), thereby generating superoxide. However, the molecular underpinnings of this process are not understood. RasGRF1, a guanine nucleotide exchange factor, is key for several forms of neuronal plasticity and interacts directly with the tail of NR2B. We investigated whether the NR2B-NMDAR/RasGRF1 pathway regulates the activity of NOX2 and whether superoxide production is required for dendritogenesis. We measured superoxide production in developing primary cultures of hippocampal neurons from 3 to 25 days in vitro (DIV) with the probe dihydroethidium (dHE). We found the highest dHE levels at early and intermediate developmental stages (3–15 DIV), when the NR2B-NMDAR expression is abundant. During these early/intermediate developmental stages, but not in mature neurons (>15 DIV), NMDAR activity is required for superoxide production. We also found that disrupting the NR2B-RasGRF1 interaction led to reduced dHE fluorescence intensity and moreover inhibited dendritic branching in hippocampal neurons. Together, our data indicate that superoxide production is induced by the NR2B-NMDARs/RasGRF1/NOX2 pathway and promotes dendritogenesis. © 2019 Wiley Periodicals, Inc.
dc.language.isoen
dc.publisherWiley-Liss Inc.
dc.subjectcultures
dc.subjectdendrites
dc.subjectneuron
dc.subjectNMDAR
dc.subjectRasGRF1
dc.subjectsuperoxide
dc.subjectchlorpheniramine maleate plus phenylephrine
dc.subjectguanine nucleotide exchange factor
dc.subjectn methyl dextro aspartic acid receptor 2B
dc.subjectRasGRF1
dc.subjectreduced nicotinamide adenine dinucleotide phosphate oxidase 2
dc.subjectsuperoxide
dc.subjectunclassified drug
dc.subjectCybb protein, rat
dc.subjectguanine nucleotide exchange factor
dc.subjectn methyl dextro aspartic acid receptor
dc.subjectNR2B NMDA receptor
dc.subjectRasgrf1 protein, rat
dc.subjectreduced nicotinamide adenine dinucleotide phosphate oxidase 2
dc.subjectsuperoxide
dc.subjectanimal cell
dc.subjectanimal cell culture
dc.subjectanimal experiment
dc.subjectArticle
dc.subjectdendritogenesis
dc.subjectdevelopmental stage
dc.subjectfemale
dc.subjecthippocampal neuronal culture
dc.subjectin vitro study
dc.subjectmorphology
dc.subjectnerve cell growth
dc.subjectnerve cell plasticity
dc.subjectnonhuman
dc.subjectprimary culture
dc.subjectpriority journal
dc.subjectrat
dc.subjectsignal transduction
dc.subjectanimal
dc.subjectdendrite
dc.subjectdendritic cell
dc.subjectgene expression regulation
dc.subjectgenetics
dc.subjectgrowth, development and aging
dc.subjecthippocampus
dc.subjectmetabolism
dc.subjectnerve cell
dc.subjectnervous system development
dc.subjectAnimals
dc.subjectDendrites
dc.subjectDendritic Cells
dc.subjectGene Expression Regulation, Developmental
dc.subjectHippocampus
dc.subjectNADPH Oxidase 2
dc.subjectNeurogenesis
dc.subjectNeuronal Plasticity
dc.subjectNeurons
dc.subjectras-GRF1
dc.subjectRats
dc.subjectReceptors, N-Methyl-D-Aspartate
dc.subjectSignal Transduction
dc.subjectSuperoxides
dc.titleSuperoxide generation via the NR2B-NMDAR/RasGRF1/NOX2 pathway promotes dendritogenesis
dc.typeArticle


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