Axon regeneration in young adult mice lacking Nogo-A/B.
After injury, axons of the adult mammalian brain and spinal cord exhibit little regeneration. It has been suggested that axon growth inhibitors, such as myelin-derived Nogo, prevent CNS axon repair. To investigate this hypothesis, we analyzed mice with a nogo mutation that eliminates Nogo-A/B expression. These mice are viable and exhibit normal locomotion. Corticospinal tract tracing reveals no abnormality in uninjured nogo-A/B(-/-) mice. After spinal cord injury, corticospinal axons of young adult nogo-A/B(-/-) mice sprout extensively rostral to a transection. Numerous fibers regenerate into distal cord segments of nogo-A/B(-/-) mice. Recovery of locomotor function is improved in these mice. Thus, Nogo-A plays a role in restricting axonal sprouting in the young adult CNS after injury.
Kim
Ji Eun
JE
Department of Neurology, Department of Neurobiology, Yale University School of Medicine, New Haven, CT 06510, USA.
Li
Shuxin
S
GrandPré
Tadzia
T
Qiu
Dike
D
Strittmatter
Stephen M
SM
D000818:Animals; D001369:Axons / Q000502:physiology*; D019771:Axotomy; D001921:Brain / Q000166:cytology; D005260:Female; D005328:Fetal Viability / Q000235:genetics; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D009043:Motor Activity / Q000502:physiology; D009185:Myelin Proteins / Q000172:deficiency* / Q000235:genetics; D009186:Myelin Sheath / Q000502:physiology; D009416:Nerve Regeneration / Q000235:genetics / Q000502:physiology; D000070798:Nogo Proteins; D010641:Phenotype; D011712:Pyramidal Tracts / Q000166:cytology / Q000473:pathology; D020127:Recovery of Function / Q000235:genetics; D013037:Spatial Behavior / Q000502:physiology; D013119:Spinal Cord Injuries / Q000235:genetics / Q000473:pathology / Q000503:physiopathology
D009185:Myelin Proteins; D000070798:Nogo Proteins; C000603201:Rtn4 protein, mouse