Bulletin of Experimental Biology and Medicine

, Volume 154, Issue 4, pp 485–488 | Cite as

Induction of S100B Gene Expression in Long-Term Potentiation in the Hippocampal CA1 Field Depends on Activity of NMDA Receptors

  • P. D. Lisachev
  • V. O. Pustylnyak
  • M. B. Shtark
  • O. I. Epstein

The effects of NMDA receptor blocker MK-801 on the increase in S100B protein mRNA content induced by long-term posttetanic potentiation in the hippocampal sections were studied. The level of S100B mRNA after 30-min tetanization in the presence of 10 μM MK-801 constituted 132% of the basal level, which was significantly (226%) lower than the control level. Hence, gene expression, induced by long-term posttetanic potentiation, in the glial cells (similarly as in the neurons) depended significantly on NMDA receptors.

Key Words

long-term potentiation CA1 S100B NMDA p53 


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    V. G. Skrebitskii and A. N. Chepkova, Usp. Fiziol. Nauk, 30, No. 4, 3–13 (1999).PubMedGoogle Scholar
  2. 2.
    A. Brunet, S. R. Datta, and M. E. Greenberg, Curr. Opin. Neurobiol., 11, No. 3, 297–305 (2001).PubMedCrossRefGoogle Scholar
  3. 3.
    E. Carafoli, L. Santella, D. Branca, and M. Brini, Crit. Rev. Biochem. Mol. Biol., 36, No. 2, 107–260 (2001).PubMedCrossRefGoogle Scholar
  4. 4.
    Y. Y. Cho, Z. He, Y. Zhang, et al., Cancer Res., 65, No. 9, 3596–3603 (2005).PubMedCrossRefGoogle Scholar
  5. 5.
    F. Conti, A. Minelli, M. Molnar, and N. C. Brecha, J. Comp. Neurol., 343, No. 4, 554–565 (1994).PubMedCrossRefGoogle Scholar
  6. 6.
    R. Donato, G. Sorci, F. Riuzzi, et al., Biochim. Biophys. Acta, 1793, No. 6, 1008–1022 (2009).PubMedCrossRefGoogle Scholar
  7. 7.
    L. M. Grover and C. Yan, J. Neurophysiol., 81, No. 6, 2814–2822 (1999).PubMedGoogle Scholar
  8. 8.
    F. S. Lee, A. H. Kim, G. Khursigara, and M. V. Chao, Curr. Opin. Neurobiol., 11, No. 3, 281–286 (2001).PubMedCrossRefGoogle Scholar
  9. 9.
    P. D. Lisachev, M. B. Shtark, O. O. Sokolova, et al., Cardiovasc. Psychiatry Neurol., 2010, Article ID 720958 (2010).Google Scholar
  10. 10.
    Y. Lu, K. Christian, and B. Lu, Neurobiol. Learn. Mem., 89, No. 3, 312–323 (2008).PubMedCrossRefGoogle Scholar
  11. 11.
    G. Perea and A. Araque, Brain Res. Rev., 63, Nos. 1–2, 93–102 (2010).PubMedCrossRefGoogle Scholar
  12. 12.
    V. O. Pustylnyak, P. D. Lisachev, M. B. Shtark, and O. I. Epstein, Brain Res., 1394, 33–39 (2011).PubMedCrossRefGoogle Scholar
  13. 13.
    S. Spange, T. Wagner, T. Heinzel, and O. H. Krämer, Int. J. Biochem. Cell Biol., 41, No. 1, 185–198 (2009).PubMedCrossRefGoogle Scholar
  14. 14.
    M. R. Vossler, H. Yao, R. D. York, et al., Cell, 89, No. 1, 73–82 (1997).PubMedCrossRefGoogle Scholar
  15. 15.
    X. Zhang, J. Zhang, and C. Chen, Biochem. Biophys. Res. Commun., 383, No. 3, 326–330 (2009).PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 2013

Authors and Affiliations

  • P. D. Lisachev
    • 1
  • V. O. Pustylnyak
    • 2
    • 3
  • M. B. Shtark
    • 2
  • O. I. Epstein
    • 4
  1. 1.Designing and Technological Institute of Computer EngineeringSiberian Division of the Russian Academy of SciencesNovosibirskRussia
  2. 2.Institute of Molecular Biology and BiophysicsSiberian Division of the Russian Academy of Medical SciencesNovosibirskRussia
  3. 3.Novosibirsk State UniversityNovosibirskRussia
  4. 4.Materia Medica HoldingMoscowRussia

Personalised recommendations