Mice lacking L1 have reduced CGRP fibre in-growth into spinal transection lesions.
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.
Deumens
Ronald
R
Pain 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
Lübbers
Miriam
M
Jaken
Robby J P
RJ
Meijs
Matthijs F L
MF
Thurlings
Rogier M
RM
Honig
Wiel M M
WM
Schachner
Melitta
M
Brook
Gary A
GA
Joosten
Elbert A J
EA
D000818:Animals; D001369:Axons / Q000473:pathology / Q000502:physiology; D015740:Calcitonin Gene-Related Peptide / Q000502:physiology*; D005260:Female; D005838:Genotype; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009412:Nerve Fibers / Q000473:pathology / Q000502:physiology*; D039842:Neural Cell Adhesion Molecule L1 / Q000172:deficiency* / Q000235:genetics*; D009475:Neurons, Afferent / Q000473:pathology / Q000502:physiology; D013119:Spinal Cord Injuries / Q000235:genetics* / Q000473:pathology*
D039842:Neural Cell Adhesion Molecule L1; D015740:Calcitonin Gene-Related Peptide