ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
No evidence for chronic demyelination in spared axons after spinal cord injury in a mouse.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
65 citing papers in PubMed, 132 citations in OpenAlex.
- Eccentric rehabilitation induces white matter plasticity and sensorimotor recovery in chronic spinal cord injury.Experimental neurology · 2021Trial
- Review
- A computational roadmap to activity-dependent myelination.Frontiers in computational neuroscience · 2026Article
- Targeting Remyelination in Spinal Cord Injury: Insights and Emerging Therapeutic Strategies.CNS neuroscience & therapeutics · 2024Review
- Article
- Impact of Extracellular Current Flow on Action Potential Propagation in Myelinated Axons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Remyelination in the Central Nervous System.Cold Spring Harbor perspectives in biology · 2024Review
- Enhanced oxidative phosphorylation, re-organized intracellular signaling, and epigenetic de-silencing as revealed by oligodendrocyte translatome analysis after contusive spinal cord injury.Scientific reports · 2023Article
- Fidgetin interacting with microtubule end binding protein EB3 affects axonal regrowth in spinal cord injury.Neural regeneration research · 2023Article
- Article
- Myelin dystrophy in the aging prefrontal cortex leads to impaired signal transmission and working memory decline: a multiscale computational study.bioRxiv : the preprint server for biology · 2023Article
- Article
- Forced Remyelination Promotes Axon Regeneration in a Rat Model of Spinal Cord Injury.International journal of molecular sciences · 2022Article
- Restoring mitochondrial cardiolipin homeostasis reduces cell death and promotes recovery after spinal cord injury.Cell death & disease · 2022Article
- Article
- Article
- Neuron-Oligodendrocyte Interactions in the Structure and Integrity of Axons.Frontiers in cell and developmental biology · 2021Review
- Red-Light (670 nm) Therapy Reduces Mechanical Sensitivity and Neuronal Cell Death, and Alters Glial Responses after Spinal Cord Injury in Rats.Journal of neurotrauma · 2020Article
- Improved locomotor recovery after contusive spinal cord injury in Bmal1Scientific reports · 2020Article
- Therapeutic repair for spinal cord injury: combinatory approaches to address a multifaceted problem.EMBO molecular medicine · 2020Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The pattern of remyelination after traumatic spinal cord injury remains elusive, with animal and human studies reporting partial to complete demyelination followed by incomplete remyelination. In the present study, we found that spared rubrospinal tract (RST) axons of passage traced with actively transported dextrans and examined caudally to the lesion 12 weeks after mouse spinal cord contusion injury were fully remyelinated. Spared axons exhibited a marginally reduced myelin thickness and significantly shorter internodes. CASPR (contactin-associated protein) and K(v)1.2 channels were used to identify internodes and paranodal protein distribution properties were used as an index of myelin integrity. This is the first time the CNS myelin internode length was measured in a mouse. To better understand the significance of shortened internodes and thinner myelin in spared axons, we modeled conduction properties using McIntyre's et al. model of myelinated axons. Mathematical modeling predicted a 21% decrease in the conduction velocity of remyelinated RST axons attributable to shortened internodes. To determine whether demyelination could be present on axons exhibiting a pathological transport system, we used the retroviral reporter system. Virally delivered green fluorescent protein unveiled a small population of dystrophic RST axons that persist chronically with evident demyelination or abnormal remyelination. Collectively, these data show that lasting demyelination in spared axons is rare and that remyelination of axons of passage occurs in the chronically injured mouse spinal cord.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.