ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019
p75NTR and DR6 Regulate Distinct Phases of Axon Degeneration Demarcated by Spheroid Rupture.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- A Dose-Response Study on Human FGF21 to Inhibit Necrosis, Spectrin Breakdown, and to Increase Intracellular Cold Shock Proteins in Cultured Cortical Neurons Subjected to Oxygen-Glucose Deprivation Injury.Molecular neurobiology · 2026Article
- Taming the "death receptor": translating the first-in-class p75Journal of translational medicine · 2026Review
- Myelin sheaths persist for weeks following axon degeneration.Science advances · 2026Article
- The Intricate Role of Caspase-6 and Death Receptor-6 in Neurodegenerative Diseases.Cell biochemistry and biophysics · 2026Review
- Epothilone B stabilizes microtubules via Tau to protect retinal ganglion cells and promote axon regeneration.Cell communication and signaling : CCS · 2026Article
- Chr:17q21.31 locus risk haplotype H1 susceptibility to ferroptosis is mediated by endolysosomal pathway.Cell death & disease · 2025Article
- Axonal spheroids are regulated by Schwann cells after peripheral nerve injury.bioRxiv : the preprint server for biology · 2024Article
- ProNGF elicits retrograde axonal degeneration of basal forebrain neurons through p75Science signaling · 2024Article
- Stellate Ganglia and Cardiac Sympathetic Overactivation in Heart Failure.International journal of molecular sciences · 2022Review
- Axonal spheroids in neurodegeneration.Molecular and cellular neurosciences · 2021Review
- The sympathetic nervous system in development and disease.Nature reviews. Neuroscience · 2021Review
- Article
- Regulation of degenerative spheroids after injury.Scientific reports · 2020Article
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
The regressive events associated with trophic deprivation are critical for sculpting a functional nervous system. After nerve growth factor withdrawal, sympathetic axons derived from male and female neonatal mice maintain their structural integrity for ∼18 h (latent phase) followed by a rapid and near unison disassembly of axons over the next 3 h (catastrophic phase). Here we examine the molecular basis by which axons transition from latent to catastrophic phases of degeneration following trophic withdrawal. Before catastrophic degeneration, we observed an increase in intra-axonal calcium. This calcium flux is accompanied by p75 neurotrophic factor receptor-Rho-actin-dependent expansion of calcium-rich axonal spheroids that eventually rupture, releasing their contents to the extracellular space. Conditioned media derived from degenerating axons are capable of hastening transition into the catastrophic phase of degeneration. We also found that death receptor 6, but not p75 neurotrophic factor receptor, is required for transition into the catastrophic phase in response to conditioned media but not for the intra-axonal calcium flux, spheroid formation, or rupture that occur toward the end of latency. Our results support the existence of an interaxonal degenerative signal that promotes catastrophic degeneration among trophically deprived axons.
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