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Updated: Jul 14, 2026
Controlled Cervical Laceration Injury in Mice
Published on: May 9, 2013
Mice lacking L1 have reduced CGRP fibre in-growth into spinal transection lesions
Ronald Deumens1, Miriam Lübbers, Robby J P Jaken
1Pain Management and Research Center, Department of Anesthesiology, Academic Hospital Maastricht, and European Graduate School of Neuroscience (EURON), Maastricht University, P.O. Box 616, 6200 MD, Maastricht, The Netherlands. r.deumens@np.unimaas.nl
Abstract:
Repair strategies for spinal cord injury often focus on promoting regeneration of injured axons and stimulating subsequent functional recovery. Although many of these strategies have proven their merits, less is known about potential unwanted side-effects, such as sprouting of nociceptive CGRP immunoreactive axons, which may bring about pain-related behavior. Sprouting of CGRP axons into lesion sites spontaneously occurs after spinal cord injury (SCI). Using L1-deficient mice we show a reduction of such CGRP growth response. This reduction was specific for CGRP axons since the overall neurofilament positive fibre in-growth into the spinal lesion site was not affected. Our results may have important implications on the development and assessment of repair strategies that should not only stimulate functional recovery, but also prevent the development of pain or autonomic dysreflexia.
Insights
Spinal cord injury (SCI) repair strategies may cause pain due to nerve sprouting. L1-deficient mice showed reduced nerve sprouting into SCI sites, suggesting a way to prevent pain after injury.
Area of Science:
- Neuroscience
- Regenerative Medicine
- Spinal Cord Injury Research
Background:
- Spinal cord injury (SCI) repair strategies aim to promote axonal regeneration and functional recovery.
- Potential side effects, like the sprouting of calcitonin gene-related peptide (CGRP) immunoreactive axons, can lead to pain-related behaviors.
- This sprouting of CGRP axons into lesion sites occurs spontaneously after SCI.
Purpose of the Study:
- To investigate the role of L1 in the sprouting of CGRP axons after spinal cord injury.
- To determine if reducing CGRP axon sprouting can mitigate pain-related behaviors post-SCI.
- To assess the impact of L1 deficiency on overall nerve fiber regeneration into the spinal lesion site.
Main Methods:
- Utilized L1-deficient mice models to study spinal cord injury.
- Analyzed the sprouting of CGRP immunoreactive axons into the lesion site.
- Quantified overall neurofilament-positive fiber ingrowth to assess general regeneration.
Main Results:
- L1 deficiency significantly reduced the sprouting of CGRP axons into the spinal lesion site after injury.
- This reduction in CGRP axon sprouting was specific and did not affect the overall neurofilament-positive fiber ingrowth.
- The findings suggest L1 plays a role in the aberrant sprouting of nociceptive fibers post-SCI.
Conclusions:
- The study highlights a potential mechanism for pain development after SCI related to CGRP axon sprouting.
- L1 deficiency offers a model to study the reduction of this specific type of nerve sprouting.
- Future SCI repair strategies should consider preventing pain and autonomic dysreflexia alongside promoting functional recovery.
