Cited by 133Spinal Cord Injury ResearchNerve injury and regenerationMultiple Sclerosis Research Studies

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No Evidence for Chronic Demyelination in Spared Axons after Spinal Cord Injury in a Mouse

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Lasiene, Jurate, Shupe, Larry, Perlmutter, Steve, Horner, Philip·2008·The Journal of Neuroscience

DOI 10.1523/jneurosci.4756-07.2008PMC PMC2631430

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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.

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Authors: Lasiene, J., Shupe, L., Perlmutter, S., & Horner, P.
Affiliations: University of Washington (US)
ORCID: Shupe, Larry
Perlmutter, Steve
Horner, Philip
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
DOI: 10.1523/jneurosci.4756-07.2008
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: cc-by-nc-sa
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 183 d)
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 › Clinical Neurology › Spinal Cord Injury Research
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
Health Sciences › Medicine › Clinical Neurology › 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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No Evidence for Chronic Demyelination in Spared Axons after Spinal Cord Injury in a Mouse

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