Temporal and spatial patterns of Kv1.1 and Kv1.2 protein and gene expression in spinal cord white matter after acute and chronic spinal cord injury in rats: implications for axonal pathophysiology after neurotrauma
Abstract
After spinal cord injury (SCI), surviving white matter axons display axonal dysfunction associated with demyelination and altered K+ channel activity. To clarify the molecular basis of posttraumatic axonal pathophysiology after SCI, we investigated the changes in expression and distribution of the axonal K+ channel subunits Kv1.1 and Kv1.2 in spinal cord white matter after in vivo SCI in the rat. Using Western blot analysis, we found an increased expression of Kv1.1 and Kv1.2 at 2 and 6 weeks after SCI. By real-time PCR we observed an increase in Kv1.1 and Kv1.2 mRNA levels 1 day after SCI, which persisted until 6 weeks. Confocal immunohistochemistry showed a markedly dispersed labelling of Kv1.1 and Kv1.2 along the injured axons, in contrast to the tight localization of these channels to the juxtaparanodes of noninjured axons. This redistribution of Kv1.1 and Kv1.2 occurred as early as 1 h postinjury along some injured axons, and persisted at 6 weeks postinjury. In parallel with the redistribution of Kv1.1 and 1.2, contactin-associated protein (Caspr), which is normally confined to a paranodal location, also displayed a more diffuse distribution along the injured spinal cord axons. Our results suggest that the increased expression of Kv1.1 and Kv1.2 proteins is transcriptionally regulated. In contrast, the redistribution of the axonal K+ channel subunits occurs very early postinjury and probably reflects a disruption of the juxtaparanodal axonal region due to physical trauma…
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Healthy, myelinated axons contain organized clusters of proteins within and surrounding the node of Ranvier, including Caspr in the paranode and Kv1.2 in the juxtaparanode.
“Healthy, myelinated axons contain organized clusters of proteins within and surrounding the node of Ranvier, which includes contactin associated protein (Caspr) in the paranode and the potassium voltage-gated ion channel, Kv1.2, in the juxtaparanode [60–62].”
From Delayed short-term tamoxifen treatment does not promote remyelination or neuron sparing after spinal cord injury (2020) · cites this paper as [61]
After SCI, axons become demyelinated and lose structured nodal domains as Caspr and Kv1.2 spread along the axon.
“After SCI, axons become demyelinated and lose these structured nodal domains as Caspr and Kv1.2 spread along the axon [61, 63].”
From Delayed short-term tamoxifen treatment does not promote remyelination or neuron sparing after spinal cord injury (2020) · cites this paper as [61]
Injury to the spinal cord results in OL death and demyelination, which impairs neuronal signaling and limits functional recovery.
“Injury to the spinal cord results in OL death and demyelination, which impairs neuronal signaling and limits functional recovery [13, 61, 77, 78].”
From Delayed short-term tamoxifen treatment does not promote remyelination or neuron sparing after spinal cord injury (2020) · cites this paper as [61]
Cites
Peles, E., Nativ, M., Lustig, M., Grumet, M., Schilling, J., Martinez, R., Plowman, G. D., & Schlessinger, J. (1997) · The EMBO Journal · doi:10.1093/emboj/16.5.978 · Cited by 400 · see citing works
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No evidence for chronic demyelination in spared axons after spinal cord injury in a mouse
Lasiene, J., Shupe, L., Perlmutter, S., & Horner, P. (2008) · The Journal of Neuroscience · doi:10.1523/jneurosci.4756-07.2008 · Cited by 133 · see citing works
Eftekharpour, E., Karimi-Abdolrezaee, S., Wang, J., El Beheiry, H., Morshead, C., & Fehlings, M. G. (2007) · The Journal of Neuroscience · doi:10.1523/jneurosci.0273-07.2007 · Cited by 110 · see citing works
Self-citationPukos, N., & McTigue, D. M. (2020) · PLOS ONE · doi:10.1371/journal.pone.0235232 · Cited by 9 · see citing works
- Authors
- Karimi‐Abdolrezaee, S., Eftekharpour, E., & Fehlings, M. G.
- Affiliations
- University of Toronto (CA)
- Corresponding author
- Fehlings, Michael G.
- Venue
- European Journal of Neuroscience
- Publisher
- Wiley
- Published
- 2004-01-30
- Volume
- 19
- Issue
- 3
- Pages
- 577-589
- ISSN
- 0953-816X (ISSN-L)
- 1460-9568
- OpenAlex
- W2030563395
- Cited by
- 91
- References
- 1
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 3 · 2023: 4 · 2022: 2 · 2021: 5 · 2020: 3 · 2019: 2 · 2018: 3 · 2017: 3 · 2016: 2 · 2015: 4 · 2014: 5 · 2013: 8 · 2012: 7
- FWCI
- 2.88
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- European Journal of Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Spinal Cord Injury Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Keywords
- Kv1.1, Kv1.2, potassium channel subunits, spinal cord injury, spinal cord white matter, demyelination, Caspr, gene expression, neurotrauma
- MeSH terms
- Actins, Animals, Axons, Female, Immunohistochemistry, Laminectomy, RNA, Messenger, Spinal Cord Injuries, Staining and Labeling, Time Factors, Tubulin, Blotting, Western, Potassium Channels, Cell Adhesion Molecules, Neuronal, Gene Expression, Neurofilament Proteins, Rats, Wistar, Reverse Transcriptase Polymerase Chain Reaction, Potassium Channels, Voltage-Gated, Rats, Kv1.1 Potassium Channel, Kv1.2 Potassium Channel
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