Bulletin of Experimental Biology and Medicine

, Volume 146, Issue 4, pp 485–488 | Cite as

Heterokaryon Formation as a Method for Neuron Regeneration in Postischemic Injury to Cerebral Cortex in Rats

  • A. A. Paltsyn
  • E. G. Kolokol’chikova
  • N. B. Konstantinova
  • G. A. Romanova
  • F. M. Shakova
  • A. A. Kubatiev
Morphology and Pathomorphology

Rat prefrontal cortex was examined by light and electron microscopy after stroke induced by photothrombosis. An appreciable number of binuclear neurons with morphologically similar and different nuclei was detected in the perifocal zone and adjacent intact tissue. The satellite oligodendrocyte nucleus was frequently the second nucleus in binuclear neuron. Control specimens also had binuclear neurons, but their number was much lower. It is hypothesized that neuron fusion normally and after injury is a manifestation of physiological and reparative regeneration of these cells.

Key Words

cell fusion neuron heterokaryon nervous system regeneration 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    G. A. Romanova, Dysregulation Pathology [in Russian], Moscow (2002), P. 605–615.Google Scholar
  2. 2.
    M. Alvarez-Dolado, R. Pardal, J. M. Garcia-Verdugo, et al., Nature, 425, 968–973 (2003).PubMedCrossRefGoogle Scholar
  3. 3.
    T. R. Brazelton, F. M. Rossi, G. I. Keshet, and H. M. Blau, Science, 290, 1775–1779 (2000).PubMedCrossRefGoogle Scholar
  4. 4.
    E. Gussoni, R. R. Bennett, K. R. Muskiewicz, et al., J. Clin. Invest., 110, No. 6, 807–814 (2002).PubMedGoogle Scholar
  5. 5.
    E. Mezey, K. J. Chandross, G. Harta, et al., Science, 290, 1779–1782 (2000).PubMedCrossRefGoogle Scholar
  6. 6.
    E. Mezey, Sh. Key, G. Vogelsang, et al., Proc. Natl. Acad. Sci. USA, 100, No. 3, 1364–1369 (2003).PubMedCrossRefGoogle Scholar
  7. 7.
    J. Priller, D. Persons, F. Klett, et al., J. Cell. Biol., 155, No. 5, 733–738 (2001).PubMedCrossRefGoogle Scholar
  8. 8.
    N. Terada, T. Hamazaki, M. Oka, et al., Nature, 416, 542–545 (2002).PubMedCrossRefGoogle Scholar
  9. 9.
    G. Vassilopoulos, P. R. Wang, and D. W. Russel, Ibid., 422, 901–904 (2003).Google Scholar
  10. 10.
    X. Wang, H. Willenbring, Y. Akkari, et al., Ibid, 897–901.Google Scholar
  11. 11.
    B. D. Watson, W. D. Dietrich, R. Busto, et al., Ann. Neurol., 17, No. 5, 497–504 (1985).PubMedCrossRefGoogle Scholar
  12. 12.
    J. M. Weimann, C. A. Charlton, T. R. Brazelton, et al., Proc. Natl. Acad. Sci. USA, 100, 4, 2088–2093 (2003).PubMedCrossRefGoogle Scholar
  13. 13.
    J. M. Weimann, C. B. Johansson, A. Trejo, and H. M. Blau, Nat. Cell Biol., 5, No. 11, 959–966 (2003).PubMedCrossRefGoogle Scholar
  14. 14.
    Q. L. Ying, S. Nichols, E. P. Evans, and A. G. Smith, Nature, 416, 545–548 (2002).PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media, Inc. 2008

Authors and Affiliations

  • A. A. Paltsyn
    • 1
  • E. G. Kolokol’chikova
    • 1
  • N. B. Konstantinova
    • 1
  • G. A. Romanova
    • 1
  • F. M. Shakova
    • 1
  • A. A. Kubatiev
    • 1
  1. 1.Institute of General Pathology and PathophysiologyRussian Academy of Medical SciencesMoscowRussia

Personalised recommendations