Axon regeneration in young adult mice lacking Nogo-A/B

Neuron. 2003 Apr 24;38(2):187-99. doi: 10.1016/s0896-6273(03)00147-8.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Axons / physiology*
  • Axotomy
  • Brain / cytology
  • Female
  • Fetal Viability / genetics
  • Male
  • Mice
  • Mice, Knockout
  • Motor Activity / physiology
  • Myelin Proteins / deficiency*
  • Myelin Proteins / genetics
  • Myelin Sheath / physiology
  • Nerve Regeneration* / genetics
  • Nerve Regeneration* / physiology
  • Nogo Proteins
  • Phenotype
  • Pyramidal Tracts / cytology
  • Pyramidal Tracts / pathology
  • Recovery of Function / genetics
  • Spatial Behavior / physiology
  • Spinal Cord Injuries / genetics
  • Spinal Cord Injuries / pathology
  • Spinal Cord Injuries / physiopathology


  • Myelin Proteins
  • Nogo Proteins
  • Rtn4 protein, mouse