Journal home
Advance online publication
Current issue
Archive
Press releases
Supplements
Focuses
Guide to authors
Online submissionOnline submission
For referees
Free online issue
Contact the journal
Subscribe
Advertising
work@npg
Reprints and permissions
About this site
For librarians
 
NPG Resources
Nature
Nature Reviews
Nature Immunology
Nature Cell Biology
Nature Genetics
news@nature.com
Nature Conferences
Dissect Medicine
NPG Subject areas
Biotechnology
Cancer
Chemistry
Clinical Medicine
Dentistry
Development
Drug Discovery
Earth Sciences
Evolution & Ecology
Genetics
Immunology
Materials Science
Medical Research
Microbiology
Molecular Cell Biology
Neuroscience
Pharmacology
Physics
Browse all publications
Article
Nature Medicine  3, 73 - 76 (1997)
doi:10.1038/nm0197-73

Apoptosis and delayed degeneration after spinal cord injury in rats and monkeys

Maria J. Crowe, Jacqueline C. Bresnahan, Sheri L. Shuman, Jeffery N. Masters & Michael S. Crowe

 Department of Cell Biology, Neurobiology, and Anatomy; Division of Neuwsurgery; Neuwbiotechnology Center, and Neuroscience Program, The Ohio State University College of Medicine, 333 West 10th Avenue, Columbus, Ohio 43210, USA

 M.J.C. present address: Shriners Hospitals for Crippled Children Burns Institute, 3229 BurnetAvenue, Cincinnati, Ohio 45229-3095, USA

 Correspondence should be addressed to M.S.B.

Apoptosis is a morphologically defined form of programmed cell death seen in a variety of circumstances, including immune cell selection, carcinogenesis and development1,2. Apoptosis has very recently been seen after ischemic or traumatic injury to the central nervous system (CNS)3−5, suggesting that active cell death as well as passive necrosis may mediate damage after CNS injury. After spinal cord injury (SCI) in the rat, typical posttraumatic necrosis occurred, but in addition, apoptotic cells were found from 6 hours to 3 weeks after injury, especially in the spinal white matter. Apoptotic cells were positive for oligodendrocyte markers. After SCI in monkeys, apoptotic cells were found within remote degenerating fiber tracts. Both secondary degeneration at the site of SCI and the chronic demyelination of tracts away from the injury appear to be due in part to apoptosis. As cytokines have been shown to mediate oligodendrocyte death in vitro6, it seems likely that chronic demyelination after CNS injury shares features with chronic degenerative disorders like multiple sclerosis.

REFERENCES
  1. Majno, G. & Joris, J., Apotosis, oncosis and necrosis: An overview of Cell death. Am. J. Pathol. 146, 3−15 (1995). | PubMed  | ISI | ChemPort |
  2. Raff, M.C. et al. Programmed Cell death and the control of Cell survival: Lessons from the nervous system. Science 262, 695−700 (1993). | PubMed  | ISI | ChemPort |
  3. Johnson, E.M., Greenlund, L.J. & Hsu, C.Y. Neuronal apoptosis: Current understanding of molecular mechanisms and potential role in ischemic brain injury. J. Neurotmuma 5, 843−852 (1995).
  4. Rink, A. et al. Evidence of apoptotic Cell death after experimental traumatic brain injury in the rat. Am. J. Pathol. 147, 1575−1583 (1995). | PubMed  | ISI | ChemPort |
  5. Li, G.L. et al. Apoptosis and expression of bcl-2 after compression trauma to rat spinal cord. J. Exp. Neuropathol. Exp. Neural. 55, 280−289 (1996). | ChemPort |
  6. D'Souza, S.D., Alinauskas, K., McCrea, E., Goodyer, C. & Antel, J.P. Differential susceptibility of human CNS-derived Cell populations to TNF-dependent and independent immune-mediated injury. J. Neurosci. 15, 7293−7300 (1995). | PubMed  | ChemPort |
  7. Hall, E.D., Yonkers, P.A., Andress, P.K., Cox, J.W. & Anderson, D.K. J. Neurotrauma 9 (Suppl.), S425−S442 (1992). | PubMed  | ISI |
  8. Bracken, M.B. et al. A randomized controlled trial of methylprednisolone or naloxone in the treatment of acute spinal cord injury. N. Engl. J. Med. 322, 1405−1411 (1990). | PubMed  | ISI | ChemPort |
  9. Constantini, S. & Young, W. The effects of methylprednisolone and the ganglioside GM1 on acute spinal cord injury in rats. J. Neurosurg. 80, 97−111 (1994). | PubMed  | ISI | ChemPort |
  10. Basso, D.M., Beattie, M.S. & Bresnahan, J.C. Histological and locomotor studies of graded spinal cord contusion using the NYU weight-drop device: Comparison with transection. Exp. Neurol. 139, 244−256 (1996). | Article | PubMed  | ISI | ChemPort |
  11. Gavrieli, Y., Sherman, Y. & Ben-Sasson, S.A. Identification of programmed Cell death in situ via specific labeling of nuclear DNA fragmentation. J. Cell. Biol. 119, 493−501 (1992). | Article | PubMed  | ISI | ChemPort |
  12. Greenlund, L.J.S., Deckwerth, T.L. & Johnson, E.M., Jr, Superoxide dismutase delays neuronal apoptosis: A role for reactive oxygen species in programmed Cell death. Neuron 14, 303−315 (1995). | PubMed  | ISI | ChemPort |
  13. Barres, B.A., Jacobson, M.D., Schmid, R., Sendtner, M. & Raff, M.C. Does oligo-dendrocyte survival depend on axons? Current Biology 3, 489−497 (1993). | ISI | ChemPort |
  14. Crowe, M.J. et al. Morphological evidence suggesting apoptotic nuclei in spinal cord injury. Soc. Neurosci. Abstr. 21, 232 (1995).
  15. Bresnahan, J.C.Martin, G.F., King, J.S. & Yashon, D. A neuroanatomical analysis of spinal cord injury in the rhesus monkey (Macaca mulatta), J. Neurol. Sci. 28, 521−542 (1976). | Article | PubMed  | ISI | ChemPort |
  16. Dusart, I. & Schwab, M.E., Cell death and the inflammatory reaction after dorsal hemisection of the rat spinal cord. Eur. J. Neurosci. 6, 712−724 (1994). | PubMed  | ISI | ChemPort |
  17. Popovich, P.G., Wei, P. & Stokes, B.T., The Cellular inflammatory response after spinal cord injury in Sprague-Dawley and Lewis rats. J. Comp. Neurol. (in the press).
  18. Bresnahan, J.C. An electron microscopic analysis of axonal alterations following blunt contusion of the spinal cord of the rhesus monkey (Macaca mulatta). J. Neurol. Sci. 37, 59−82 (1978). | Article | PubMed  | ISI | ChemPort |
  19. Friedman, B., Hockfield, S., Black, J.A., Woodruff, K.A. & Waxman, S.G. In situ demonstration of mature oligodendrocytes and their processes: An immunocyto-chemical study with a new monoclonal antibody, rip. Glia 2, 380−390. | PubMed  | ChemPort |
  20. Bhat, R.V. et al. Expression of the APC tumor suppressor protein in oligodendroglia. Glia 17, 169−174. | PubMed  | ChemPort |
  21. Blight, A.R. Macrophages and inflammatory damage in spinal cord injury, J. Neurotrauma 9 (Suppl.), S83−S91 (1992). | PubMed  | ISI |
  22. Bunge, R.P. Clinical implications of recent advances in neurotrauma research, in The Neurobiology of CNS Trauma (ed. Salzman, S. & Faden, A.) 329−339 (Oxford Univ. Press, New York, 1994).
  23. Wood, P.L. Microglia as a unique Cellular target in the treatment of stroke: Potential neurotoxic mediators produced by activated microglia. Neurol. Res. 17, 242−248 (1995). | PubMed  | ISI | ChemPort |
  24. Louis, J.-C., Magal, E., Takayama, S. & Varon, S. CNTF protection of oligodendro-cytes against natural and tumor necrosis factor-induced Cell death. Science 259, 689−692 (1993). | PubMed  | ISI | ChemPort |
  25. Vartanian, T., Li, Y., Zhao, M. & Stefansson, K. Interferon-gamma-induced oligo-dendrocyte Cell death: Implications for the pathogenesis of multiple sclerosis. Mol. Med. 1, 732−743 (1995). | PubMed  | ISI | ChemPort |
 Top
 Top
Abstract
Previous | Next
Table of contents
Download PDFDownload PDF
Send to a friendSend to a friend
Save this linkSave this link

Open Innovation Challenges

  • Single-cell Analysis Platform

    • Deadline: Dec 02 2009
    • Reward: $5,000 USD

    This Challenge is looking for novel approaches to analyzing changes at a single-cell level. This is...

  • Delayed Burst Release

    • Deadline: Mar 04 2010
    • Reward: $20,000 USD

    A mechanism is desired that will have little or no release until triggered and then substantially re...

naturejobs

References
Export citation
Export references
natureproducts

Search buyers guide:

 
ADVERTISEMENT
 
Nature Medicine
ISSN: 1078-8956
EISSN: 1546-170X
Journal home | Advance online publication | Current issue | Archive | Press releases | Supplements | Focuses | For authors | Online submission | For referees | Free online issue | About the journal | Contact the journal | Subscribe | Advertising | work@npg | Reprints and permissions | About this site | For librarians
Nature Publishing Group, publisher of Nature, and other science journals and reference works©1997 Nature Publishing Group | Privacy policy