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.
Pubmed ID: 12718854 RIS Download
Animals | Axons | Axotomy | Brain | Female | Fetal Viability | Male | Mice | Mice, Knockout | Motor Activity | Myelin Proteins | Myelin Sheath | Nerve Regeneration | Nogo Proteins | Phenotype | Pyramidal Tracts | Recovery of Function | Spatial Behavior | Spinal Cord Injuries