Premium
Corticospinal tract regeneration after spinal cord injury in receptor protein tyrosine phosphatase sigma deficient mice
Author(s) -
Fry Elizabeth J.,
Chag Melanie J.,
LópezVales Rubèn,
Tremblay Michel L.,
David Samuel
Publication year - 2010
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.20934
Subject(s) - axon , corticospinal tract , regeneration (biology) , biology , spinal cord , spinal cord injury , protein tyrosine phosphatase , chondroitin sulfate proteoglycan , glial scar , myelin , crush injury , sciatic nerve , neurite , microbiology and biotechnology , neuroscience , sciatic nerve injury , anatomy , central nervous system , signal transduction , chondroitin sulfate , medicine , in vitro , glycosaminoglycan , biochemistry , surgery , magnetic resonance imaging , diffusion mri , radiology
Abstract Receptor protein tyrosine phosphatase sigma (RPTPσ) plays a role in inhibiting axon growth during development. It has also been shown to slow axon regeneration after peripheral nerve injury and inhibit axon regeneration in the optic nerve. Here, we assessed the ability of the corticospinal tract (CST) axons to regenerate after spinal hemisection and contusion injury in RPTPσ deficient (RPTPσ −/− ) mice. We show that damaged CST fibers in RPTPσ −/− mice regenerate and appear to extend for long distances after a dorsal hemisection or contusion injury of the thoracic spinal cord. In contrast, no long distance axon regeneration of CST fibers is seen after similar lesions in wild‐type mice. In vitro experiments indicate that cerebellar granule neurons from RPTPσ −/− mice have reduced sensitivity to the inhibitory effects of chondroitin sulfate proteoglycan (CSPG) substrate, but not myelin, which may contribute to the growth of CST axons across the CSPG‐rich glial scar. Our data suggest that RPTPσ may function to prevent axonal growth after injury in the adult mammalian spinal cord and could be a target for promoting long distance regeneration after spinal cord injury. © 2009 Wiley‐Liss, Inc.