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Activation of Rho in the injured axons following spinal cord injury
Author(s) -
Madura Tomas,
Yamashita Toshihide,
Kubo Tateki,
Fujitani Masashi,
Hosokawa Ko,
Tohyama Masaya
Publication year - 2004
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1038/sj.embor.7400117
Subject(s) - neurite , myelin , central nervous system , spinal cord injury , neuroscience , spinal cord , biology , microbiology and biotechnology , myelin associated glycoprotein , nervous system , axon , receptor , low affinity nerve growth factor receptor , cerebellum , oligodendrocyte , endogeny , neurotrophin , in vitro , endocrinology , biochemistry
Axons of the adult central nervous system have very limited ability to regenerate after injury. This inability may be, at least partly, attributable to myelin‐derived proteins, such as myelin‐associated glycoprotein, Nogo and oligodendrocyte myelin glycoprotein. Recent evidence suggests that these proteins inhibit neurite outgrowth by activation of Rho through the neurotrophin receptor p75 NTR /Nogo receptor complex. Despite rapidly growing knowledge on these signals at the molecular level, it remained to be determined whether Rho is activated after injury to the central nervous system. To assess this question, we establish a new method to visualize endogenous Rho activity in situ . After treatment of cerebellar granular neurons with the Nogo peptide in vitro , Rho is spatially activated and colocalizes with p75 NTR . Following spinal cord injury in vivo , massive activation of Rho is observed in the injured neurites. Spatial regulation of Rho activity may be necessary for axonal regulation by the inhibitory cues.