Does Chronic Remyelination Occur for All Spared Axons after Spinal Cord Injury in Mouse?

The Journal of Neuroscience, 2008 · DOI: 10.1523/JNEUROSCI.2533-08.2008 · Published: August 20, 2008

Spinal Cord Injury Regenerative Medicine Neurology

Simple Explanation

Spinal cord injury often leads to the loss of myelin, which is crucial for nerve signal transmission. This review discusses a study that investigated whether axons, the long fibers of nerve cells, that survive spinal cord injury are chronically demyelinated, meaning they lack myelin over the long term. The reviewed study by Lasiene et al. (2008) found that in mice, rubrospinal tract axons capable of active transport showed complete remyelination 12 weeks after spinal cord injury. This suggests that chronic demyelination may not be a significant issue in these spared axons. Computer simulations in the Lasiene et al. (2008) study indicated a decrease in conduction velocity in the injured axons due to changes in internodal length, but this decrease was considered unlikely to significantly affect locomotion in mice.

Study Duration

12 weeks

Participants

C57BL/6 mice

Evidence Level

Animal study

Key Findings

1
Lasiene et al. (2008) found evidence for complete remyelination of rubrospinal tract (RST) axons 12 weeks after spinal cord injury in mice.
2
Computer simulations revealed a decrease in conduction velocity (CV) of injured RST axons compared to controls, primarily due to changes in internodal length rather than myelin thickness.
3
Diffuse CASPR and Kv1.2 labeling was only detected on morphologically dystrophic axons, suggesting that intact axons of the RST were remyelinated at the 12-week time point.

Research Summary

This review discusses a study by Lasiene et al. (2008) that examined chronic demyelination in spared axons after spinal cord injury in mice, focusing on actively transporting rubrospinal tract (RST) axons. The study found that at 12 weeks post-injury, there was evidence of complete remyelination in the examined axons, suggesting that chronic demyelination may not be prevalent in spared, actively transporting axons. Computer simulations indicated a decrease in conduction velocity due to changes in internodal length, but the authors suggest this may not significantly affect locomotion in mice.

Practical Implications

Therapeutic Strategies

The findings suggest that therapies aimed at promoting chronic remyelination may be less effective if few axons remain demyelinated at chronic stages after spinal cord injury.

Axon Function

Understanding the functional consequences of reduced conduction velocity in remyelinated axons is crucial for developing effective rehabilitation strategies.

Future Research

Further studies are needed to investigate the myelin status of other spinal cord tracts, at different chronic time points, and using various labeling techniques to gain a comprehensive understanding of chronic demyelination after spinal cord injury.

Study Limitations

1
The study primarily focused on actively transporting axons, potentially overlooking demyelination in less functional axons.
2
The use of Fluoro-Ruby and BDA tracers may have preferentially labeled larger-diameter axons, potentially skewing the results.
3
The findings may not be generalizable to other spinal cord tracts or other species, such as rats, which exhibit a biphasic demyelination pattern.

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