ArticleJournal of neuroscience research2009
Sodium channelopathy induced by mild axonal trauma worsens outcome after a repeat injury.
Article in Journal of neuroscience research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
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Who cites it
56 citing papers in PubMed.
- Investigating genetic susceptibility to concussion through rare variants in ion channel and neurotransmission genes.Journal of neurology · 2026Article
- A model of axonal damage accumulation from real-world head impact exposure.Annals of biomedical engineering · 2026Article
- Unlocking therapeutic potential in traumatic brain injury: exploring microenvironmental targets, signaling pathways and translational hurdles.Inflammopharmacology · 2025Review
- Exploring Symptom Overlaps: Post-COVID-19 Neurological Syndrome and Post-Concussion Syndrome in Athletes.Biomedicines · 2024Review
- Epidemiology, Pathophysiology, and Treatment Strategies of Concussions: A Comprehensive Review.Fortune journal of health sciences · 2024Article
- Longitudinal changes in sodium concentration and in clinical outcome in mild traumatic brain injury.Brain communications · 2024Article
- Identifying the Phenotypes of Diffuse Axonal Injury Following Traumatic Brain Injury.Brain sciences · 2023Review
- Dorsal root ganglion neurons recapitulate the traumatic axonal injury of CNS neurons in response to a rapid stretchFrontiers in cellular neuroscience · 2023Article
- Concussion leads to widespread axonal sodium channel loss and disruption of the node of Ranvier.Acta neuropathologica · 2022Article
- Unraveling axonal mechanisms of traumatic brain injury.Acta neuropathologica communications · 2022Article
- Mitochondrial behavior when things go wrong in the axon.Frontiers in cellular neuroscience · 2022Review
- Amyloidogenic Processing of Amyloid Precursor Protein Drives Stretch-Induced Disruption of Axonal Transport in hiPSC-Derived Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Diverse changes in microglia morphology and axonal pathology during the course of 1 year after mild traumatic brain injury in pigs.Brain pathology (Zurich, Switzerland) · 2021Article
- Rapid and Reversible Development of Axonal Varicosities: A New Form of Neural Plasticity.Frontiers in molecular neuroscience · 2021Review
- Mechanosensation in traumatic brain injury.Neurobiology of disease · 2021Review
- The Molecular Pathophysiology of Concussion.Clinics in sports medicine · 2021Review
- Localized Axolemma Deformations Suggest Mechanoporation as Axonal Injury Trigger.Frontiers in neurology · 2020Article
- Indirect Traumatic Optic Neuropathy Induced by Primary Blast: A Fluid-Structure Interaction Study.Journal of biomechanical engineering · 2019Article
- Ion current and action potential alterations in peripheral neurons subject to uniaxial strain.Journal of neuroscience research · 2019Article
- Modelling human pathology of traumatic brain injury in animal models.Journal of internal medicine · 2019Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
There is great concern that one mild traumatic brain injury (mTBI) predisposes individuals to an exacerbated response with a subsequent mTBI. Although no mechanism has been identified, mounting evidence suggests traumatic axonal injury (TAI) plays a role in this process. By using a cell culture system, a threshold of mild TAI was found where dynamic stretch of cortical axons at strains lower than 5% induced no overt pathological changes. However, the axons were found to display an increased expression of sodium channels (NaChs) by 24 hr. After a second, identical mild injury, pathologic increases in [Ca(2+)](i) were observed, leading to axon degeneration. The central role of NaChs in this response was demonstrated by blocking NaChs with tetrodotoxin prior to the second injury, which completely abolished postinjury increases in [Ca(2+)](i). These data suggest that mild TAI induces a form of sodium channelopathy on axons that greatly exaggerates the pathophysiologic response to subsequent mild injuries.
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Registered trials
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