Lack of enhanced spinal regeneration in Nogo-deficient mice

Neuron. 2003 Apr 24;38(2):213-24. doi: 10.1016/s0896-6273(03)00225-3.


The failure of regeneration of severed axons in the adult mammalian central nervous system is thought to be due partly to the presence of endogenous inhibitors of axon regeneration. The nogo gene encodes three proteins (Nogo-A, -B, and -C) that have been proposed to contribute to this inhibition. To determine whether deletion of nogo enhances regenerative ability, we generated two lines of mutant mice, one lacking Nogo-A and -B but not -C (Nogo-A/B mutant), and one deficient in all three isoforms (Nogo-A/B/C mutant). Although Nogo-A/B-deficient myelin has reduced inhibitory activity in a neurite outgrowth assay in vitro, tracing of corticospinal tract fibers after dorsal hemisection of the spinal cord did not reveal an obvious increase in regeneration or sprouting of these fibers in either mouse line, suggesting that elimination of Nogo alone is not sufficient to induce extensive axon regeneration.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Mice
  • Mice, Inbred C57BL
  • Mice, Mutant Strains
  • Myelin Proteins / deficiency*
  • Myelin Proteins / genetics
  • Myelin Proteins / metabolism
  • Myelin Sheath / physiology
  • Nerve Regeneration / genetics
  • Nerve Regeneration / physiology*
  • Neurites / physiology
  • Nogo Proteins
  • Protein Isoforms / deficiency
  • Protein Isoforms / genetics
  • Protein Isoforms / metabolism
  • Spinal Cord / cytology
  • Spinal Cord / pathology
  • Spinal Cord / physiology*
  • Spinal Cord Injuries / genetics
  • Spinal Cord Injuries / pathology
  • Spinal Cord Injuries / physiopathology


  • Myelin Proteins
  • Nogo Proteins
  • Protein Isoforms
  • Rtn4 protein, mouse