Letter | Published:

Recovery from spinal cord injury mediated by antibodies to neurite growth inhibitors

Nature volume 378, pages 498501 (30 November 1995) | Download Citation

Subjects

Abstract

THERE is little axonal growth after central nervous system (CNS) injury in adult mammals. The administration of antibodies (IN-1) to neutralize the myelin-associated neurite growth inhibitory proteins leads to long-distance regrowth of a proportion of CNS axons after injury1–5. Our aim was: to determine if spinal cord lesion in adult rats, followed by treatment with antibodies to neurite growth inhibitors, can lead to regeneration and anatomical plasticity of other spinally projecting pathways; to determine if the anatomical projections persist at long survival intervals; and to determine whether this fibre growth is associated with recovery of function. We report here that brain stem–spinal as well as corticospinal axons undergo regeneration and anatomical plasticity after application of IN-1 antibodies. There is a recovery of specific reflex and locomotor functions after spinal cord injury in these adult rats. Removal of the sensorimotor cortex in IN-1-treated rats 2–3 months later abolished the recovered contact-placing responses, suggesting that the recovery was dependent upon the regrowth of these pathways.

Access optionsAccess options

Rent or Buy article

Get time limited or full article access on ReadCube.

from$8.99

All prices are NET prices.

References

  1. 1.

    & Nature 343, 269–272 (1990).

  2. 2.

    & Eur. J. Neurosci. 5, 1156–1171 (1993).

  3. 3.

    , , , & Nature 367, 170–173 (1994).

  4. 4.

    & Eur. J. Neurosci. 3, 825–832 (1991).

  5. 5.

    , & Brain Res. 642, 259–266 (1994).

  6. 6.

    & Expl Brain Res. 81, 25–34 (1990).

  7. 7.

    , & Expl Neurol. 119, 153–164 (1993).

  8. 8.

    & J. comp. Neurol. 244, 86–95 (1986).

  9. 9.

    , & Expl Neurol. 116, 40–51 (1992).

  10. 10.

    et al. Expl Neurol. 123, 3–16 (1993).

  11. 11.

    , , & J. comp. Neurol. 282, 355–370 (1989).

  12. 12.

    Devl Brain Res. 34, 245–263 (1987).

  13. 13.

    Devl Brain Res. 34, 265–279 (1987).

  14. 14.

    & Devl Brain Res. 9, 119–135 (1983).

  15. 15.

    & Science 217, 553–555 (1982).

  16. 16.

    & J. Physiol. 74, 165–184 (1978).

  17. 17.

    & Devl Brain Res. 9, 137–154 (1983).

  18. 18.

    , , & Expl Neurol. 107, 113–117 (1990).

  19. 19.

    , , & Expl Neurol. 56, 312–322 (1977).

  20. 20.

    , , , & Neurosci. Res. 5, 66–73 (1987).

  21. 21.

    & Brain Res. 546, 250–260 (1991).

  22. 22.

    , , & J. Motor Behav. 24, 288–296 (1992).

  23. 23.

    & Paraplegia 30, 229–236 (1992).

  24. 24.

    , & Lancet 344, 1260–1263 (1994).

  25. 25.

    , , & Eur. J. Neurosci. 7, 823–829 (1995).

Download references

Author information

Author notes

    • Lisa Schnell
    •  & Martin E. Schwab

    Brain Research Institute, University of Zurich,August Forel-Strasse 1, CH-8029 Zurich, Switzerland

Affiliations

  1. Department of Cell Biology, Division of NeurobiologyGeorgetown University Medical Center, 3900 Reservoir Road NW,Washington DC 20007, USA

    • Barbara S. Bregman
    • , Ellen Kunkel-Bagden
    • , Lisa Schnell
    • , Hai Ning Dai
    • , Da Gao
    •  & Martin E. Schwab

Authors

  1. Search for Barbara S. Bregman in:

  2. Search for Ellen Kunkel-Bagden in:

  3. Search for Lisa Schnell in:

  4. Search for Hai Ning Dai in:

  5. Search for Da Gao in:

  6. Search for Martin E. Schwab in:

About this article

Publication history

Received

Accepted

Published

DOI

https://doi.org/10.1038/378498a0

Further reading

Comments

By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.