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

The Journal of Neuroscience, 2008 · DOI: 10.1523/JNEUROSCI.4756-07.2008 · Published: April 9, 2008

Spinal Cord Injury Regenerative Medicine Neurology

Simple Explanation

This study investigates the pattern of myelin repair after spinal cord injury in mice. The researchers focused on spared axons, those that pass through the injury site, and found that these axons are mostly remyelinated 12 weeks after injury. The study found that while spared axons are remyelinated, they have shorter internodes (segments of myelin) and slightly thinner myelin compared to uninjured axons. These changes can affect how quickly signals travel along the nerves. Using mathematical models, the researchers predicted that the shorter internodes in remyelinated axons could lead to a decrease in the speed of nerve signal conduction. However, lasting demyelination was rare, primarily found in damaged axons.

Study Duration

12 weeks

Participants

Female C57BL/6 mice (8 weeks of age)

Evidence Level

Level III, Animal study

Key Findings

1
Spared rubrospinal tract (RST) axons of passage were fully remyelinated 12 weeks after mouse spinal cord contusion injury.
2
Spared axons exhibited a marginally reduced myelin thickness and significantly shorter internodes.
3
Mathematical modeling predicted a 21% decrease in the conduction velocity of remyelinated RST axons attributable to shortened internodes.

Research Summary

The study examined myelin status in spared axons after spinal cord injury in mice, finding that these axons are largely remyelinated by 12 weeks post-injury. This indicates a positive correlation between axon sparing and myelin status in the chronic phase of SCI. While the spared axons were remyelinated, they exhibited shorter internodes and slightly thinner myelin sheaths, which the study suggests could lead to a reduction in conduction velocity. This was confirmed by mathematical modeling. The research also identified a small population of dystrophic axons exhibiting demyelination or abnormal remyelination, suggesting that chronic demyelination is primarily associated with damaged or severed axons rather than spared ones.

Practical Implications

Therapeutic Strategies

Understanding the remyelination pattern of spared axons can inform the development of targeted therapies to enhance myelin repair and improve functional outcomes after SCI.

Prognostic Value

The correlation between axonal sparing and remyelination suggests that interventions focused on preserving axonal integrity may promote better myelin regeneration and functional recovery.

Conduction Velocity

The findings on reduced conduction velocity due to shorter internodes highlight the need to address both myelin thickness and internode length in remyelination strategies to optimize nerve signal transmission.

Study Limitations

1
The use of a murine model may not fully represent the anatomical complexities and injury responses seen in larger species or humans.
2
The study focused primarily on the rubrospinal tract, limiting the generalizability of the findings to other axonal tracts in the spinal cord.
3
The mathematical model used for conduction velocity predictions relies on certain assumptions about axonal properties after SCI, which may not fully reflect the in vivo conditions.

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