No evidence for chronic demyelination in spared axons after spinal cord injury in a mouse
Open accessAbstract
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.
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Myelin formed during repair of experimental demyelination or during demyelinating injury or disease is thinner on average (larger g-ratio) than myelin formed during normal development, although this is less pronounced for smaller-diameter axons such as those in the optic nerve.
“It is well documented that myelin formed during repair of experimental demyelination or during demyelinating injury or disease is thinner on average (larger g-ratio) than myelin that is formed during normal development (e.g., Lasiene et al., 2008), although this is less pronounced for smaller-diameter axons such as those in the optic nerve (Stidworthy et al., 2003).”
From Oligodendrocyte Dynamics in the Healthy Adult CNS: Evidence for Myelin Remodeling (2013) · cites this paper as Lasiene et al., 2008
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- Authors
- Lasiene, J., Shupe, L., Perlmutter, S., & Horner, P.
- Affiliations
- University of Washington (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2008-04-09
- Volume
- 28
- Issue
- 15
- Pages
- 3887-3896
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC2631430
- OpenAlex
- W2000630772
- Cited by
- 133
- References
- 63
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 6 · 2023: 10 · 2022: 4 · 2021: 4 · 2020: 6 · 2019: 9 · 2018: 7 · 2017: 13 · 2016: 5 · 2015: 7 · 2014: 10 · 2013: 12 · 2012: 10
- FWCI
- 5.67
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Washington
- Università degli Studi di Sassari
- National Institutes of Health (NSO46724)
- U.S. Public Health Service (NSO46724)
- University of California, San Diego
- National Institute of Neurological Disorders and Stroke (NS040867, R01NS046724, R01NS040867)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Spinal Cord Injury Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Keywords
- spinal cord injury, remyelination, demyelination, rubrospinal tract, myelin thickness, Caspr, axonal transport, retrograde transport, conduction velocity, dystrophic axons, mouse model
- MeSH terms
- Animals, Axons, Female, Genetic Vectors, Mice, Inbred C57BL, Models, Neurological, Myelin Sheath, Nerve Regeneration, Neural Conduction, Reaction Time, Spinal Cord, Spinal Cord Injuries, Time Factors, Transfection, Cell Adhesion Molecules, Neuronal, Lentivirus, Microscopy, Immunoelectron, Green Fluorescent Proteins, Mice, Kv1.2 Potassium Channel
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