Artemin Induced Functional Recovery And Reinnervation After Partial Nerve Injury

Pain, 2014 · DOI: 10.1016/j.pain.2013.11.007 · Published: March 1, 2014

Neurology Pain Management Regenerative Medicine & Stem Cells

Simple Explanation

The study investigates whether artemin, a neurotrophic factor, can promote peripheral nerve regeneration and functional recovery after nerve injuries in rats. Rats with different types of nerve injuries (axotomy, ligation, or crush) were treated with artemin or a control substance, and their sensory thresholds were monitored. The study found that artemin treatment led to improved sensory function and nerve regeneration, particularly in rats with nerve crush injuries.

Study Duration

6 weeks

Participants

Male SD rats

Evidence Level

Not specified

Key Findings

1
Artemin transiently reversed tactile and thermal hypersensitivity following axotomy, ligation or crush injury.
2
Artemin normalized labeling for NF200, IB4 and CGRP in nerve fibers distal to the crush injury, suggesting persistent normalization of nerve-crush induced neurochemical changes.
3
Artemin also diminished ATF3 and caspase-3 expression in the L5 DRG, suggesting persistent neuroprotective actions.

Research Summary

This study investigates the effect of systemic artemin administration on nerve regeneration and functional recovery in rats following different types of nerve injuries. The results showed that artemin transiently reverses hypersensitivity after nerve injury and promotes normalization of neurochemical markers and nerve regeneration specifically after nerve crush injury. The findings suggest that artemin may be a potential therapeutic agent for promoting nerve regeneration and functional recovery after partial nerve injuries.

Practical Implications

Therapeutic Potential

Artemin may be a potential therapeutic agent for nerve-injury induced pain.

Disease Modification

A limited period of artemin treatment elicits disease modification by promoting sensory reinnervation.

Targeted Treatment

The effects of artemin on sensory neurons, paired with the restricted expression of GFRα3 to nociceptive neurons, indicate that artemin might be an effective treatment for nerve-injury induced pain, without having broader effects that may lead to side effects observed following GDNF administration.

Study Limitations

1
The mechanisms underlying artemin-induced regeneration of injured axons are unknown.
2
The study primarily focused on nerve crush injuries, and the effects of artemin on other types of nerve injuries (axotomy, ligation) were less pronounced.
3
While the present study did not include definitive measures to determine whether artemin induced a true nerve regeneration effect in contrast to a nerve-sparing effect preventing degeneration

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