The Effect of Axon Resealing on Retrograde Neuronal Death after Spinal Cord Injury in Lamprey

Brain Sci., 2018 · DOI: 10.3390/brainsci8040065 · Published: April 14, 2018

Spinal Cord Injury Regenerative Medicine Neurology

Simple Explanation

This study investigates why some nerve cells die after spinal cord injury while others survive and regenerate, focusing on the role of axon resealing. The researchers found that larger nerve cells with bigger axons are slower to reseal after injury, allowing harmful substances to enter and trigger cell death. By speeding up the resealing process, they could prevent cell death, suggesting that axon resealing is crucial for nerve cell survival after spinal cord injury.

Study Duration

Not specified

Participants

Larval lampreys (Petromyzon marinus)

Evidence Level

Not specified

Key Findings

1
Larger reticulospinal (RS) neurons have a lower probability of axon regeneration after spinal cord transection (SCI).
2
Axon resealing time is inversely correlated with neuron size; larger axons reseal more slowly.
3
Accelerating axon resealing with polyethylene glycol (PEG) reduces retrograde neuronal apoptosis after SCI.

Research Summary

This study investigates the relationship between axon resealing, neuron size, and retrograde neuronal death after spinal cord injury (SCI) in lampreys. The findings suggest that larger neurons with slower axon resealing times are more susceptible to apoptosis after SCI and that accelerating resealing can reduce neuronal death. The distance of the axotomy from the perikaryon also influences neuronal survival, independent of axon sealing time.

Practical Implications

Therapeutic Target

Targeting axon resealing could be a potential therapeutic strategy to promote neuronal survival after SCI.

Size Matters

Neuron size and axon caliber should be considered in developing regenerative therapies for SCI.

Distance Consideration

The location of injury relative to the cell body may influence the effectiveness of therapeutic interventions.

Study Limitations

1
The study was conducted in lampreys, and the findings may not be directly applicable to mammals.
2
The mechanisms of axon sealing and the specific toxic factors involved in retrograde neuronal death were not fully elucidated.
3
The study did not fully explore the long-term effects of PEG-accelerated axon resealing on functional recovery.

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