Chronic demyelination and myelin repair after spinal cord injury in mice: a potential link for glutamatergic axon activity

Glia, 2023 · DOI: 10.1002/glia.24382 · Published: September 1, 2023

Spinal Cord Injury Genetics Neuroplasticity

Simple Explanation

This study investigates myelin repair after spinal cord injury (SCI) in mice. It looks at how the process of myelin formation and breakdown changes over time. The research shows that myelin repair continues for at least six months after the injury, but that demyelination also occurs chronically. The study also explores how the activity of axons, specifically glutamatergic axons, might influence the repair process, potentially opening new therapeutic avenues.

Study Duration

6 Months

Participants

Mice (various strains)

Evidence Level

Not specified

Key Findings

1
New myelin generation peaks at 3 months post-injury but continues for at least 6 months after SCI, indicating a prolonged remyelination response.
2
Indices of demyelination, including nodal protein spreading and Nav1.2 upregulation, are present for at least 6 months after SCI, suggesting chronic myelin breakdown.
3
Glutamatergic axon activity increases oligodendrocyte progenitor cell (OPC) contacts on spinal axons after SCI, suggesting axon function influences remyelination.

Research Summary

This study demonstrates that the injured spinal cord remains remarkably dynamic for months after injury, exhibiting continuous myelin repair and concurrent demyelination. It identifies that glutamatergic axon activity plays a role in attracting OPCs, highlighting a potential therapeutic target to enhance remyelination. Motor evoked potential amplitude increases between 4 and 10 weeks post-injury suggesting improved axonal function that is not detected by standard behavioral tests.

Practical Implications

Therapeutic potential

Targeting axon activity and/or oligodendrocyte lineage cells may promote more complete remyelination and better overall recovery after SCI.

Clinical relevance

The findings suggest that the injury environment remains conducive to repair long-term, even for those living with chronic deficits due to SCI.

Diagnostic refinement

Common gross behavioral tools used in preclinical SCI studies may not be sufficient for revealing the functional effects of dynamic, protracted and potentially subtle tissue changes after SCI.

Study Limitations

1
The study is limited to a mouse model of SCI.
2
The study did not directly assess the functional significance of remyelination on specific motor or sensory functions.
3
The study did not fully explore the long-term consequences of enhanced axon activity on myelination after SCI.

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