Activation of Rho in the injured axons following spinal cord injury.
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.
Madura
Tomas
T
Department of Anatomy and Neuroscience, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
Yamashita
Toshihide
T
Kubo
Tateki
T
Fujitani
Masashi
M
Hosokawa
Ko
K
Tohyama
Masaya
M
D000818:Animals; D001369:Axons / Q000378:metabolism*; D002531:Cerebellum / Q000378:metabolism; D008297:Male; D051379:Mice; D009185:Myelin Proteins / Q000378:metabolism; D041681:NIH 3T3 Cells; D000070798:Nogo Proteins; D051381:Rats; D013116:Spinal Cord / Q000378:metabolism* / Q000473:pathology; D013119:Spinal Cord Injuries / Q000378:metabolism* / Q000473:pathology; D020741:rho GTP-Binding Proteins / Q000378:metabolism*
D009185:Myelin Proteins; D000070798:Nogo Proteins; C000603201:Rtn4 protein, mouse; C000603197:Rtn4 protein, rat; D020741:rho GTP-Binding Proteins