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• W2912076336 endingPage "19.2019" @default.
• W2912076336 startingPage "ENEURO.0019" @default.
• W2912076336 abstract "Development of the nervous system relies on a balance between axon and dendrite growth and subsequent pruning and degeneration. The developmental degeneration of dorsal root ganglion (DRG) sensory axons has been well studied in part because it can be readily modeled by removing the trophic support by nerve growth factor (NGF) in vitro . We have recently reported that axonal fragmentation induced by NGF withdrawal is dependent on Ca 2+ , and here, we address the mechanism of Ca 2+ entry required for developmental axon degeneration of mouse embryonic DRG neurons. Our results show that the transient receptor potential vanilloid family member 1 (TRPV1) cation channel plays a critical role mediating Ca 2+ influx in DRG axons withdrawn from NGF. We further demonstrate that TRPV1 activation is dependent on reactive oxygen species (ROS) generation that is driven through protein kinase C (PKC) and NADPH oxidase (NOX)-dependent pathways that become active upon NGF withdrawal. These findings demonstrate novel mechanistic links between NGF deprivation, PKC activation, ROS generation, and TRPV1-dependent Ca 2+ influx in sensory axon degeneration." @default.
• W2912076336 created "2019-02-21" @default.
• W2912076336 creator A5017523393 @default.
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• W2912076336 creator A5085277848 @default.
• W2912076336 date "2019-01-01" @default.
• W2912076336 modified "2023-10-18" @default.
• W2912076336 title "Developmental Axon Degeneration Requires TRPV1-Dependent Ca²⁺Influx" @default.
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• W2912076336 doi "https://doi.org/10.1523/eneuro.0019-19.2019" @default.
• W2912076336 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6399429" @default.
• W2912076336 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30838324" @default.
• W2912076336 hasPublicationYear "2019" @default.
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