Bulletin of Experimental Biology and Medicine

, Volume 160, Issue 5, pp 601–604 | Cite as

Activity of the Hypothalamic–Pituitary–Adrenal System in Prenatally Stressed Male Rats on the Experimental Model of Post-Traumatic Stress Disorder

  • S. G. Pivina
  • V. V. Rakitskaya
  • V. K. Akulova
  • N. E. Ordyan

Using the experimental model of post-traumatic stress disorder (stress–restress paradigm), we studied the dynamics of activity of the hypothalamic–pituitary–adrenal system (HPAS) in adult male rats, whose mothers were daily subjected to restraint stress on days 15-19 of pregnancy. Prenatally stressed males that were subjected to combined stress and subsequent restress exhibited not only increased sensitivity of HPAS to negative feedback signals (manifested under restress conditions), but also enhanced stress system reactivity. These changes persisted to the 30th day after restress. Under basal conditions, the number of cells in the hypothalamic paraventricular nucleus of these animals expressing corticotropin-releasing hormone and vasopressin was shown to decrease progressively on days 1-30. By contrast, combined stress and restress in control animals were followed by an increase in the count of CRH-immunopositive cells in the magnocellular and parvocellular parts of the paraventricular nucleus and number of vasopressin-immunopositive cells in the magnocellular part of the nucleus (to the 10th day after restress). Our results indicate a peculiar level of functional activity of HPAS in prenatally stressed males in the stress–restress paradigm: decreased activity under basal conditions and enhanced reactivity during stress.

Key Words

post-traumatic stress disorder corticotropin-releasing hormone vasopressin prenatal stress rat 


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    N. E. Ordyan and S. G. Pivina, Ross. Fiziol. Zh., 89, No. 1, 52-59 (2003).Google Scholar
  2. 2.
    N. E. Ordyan, S. G. Pivina, V. I. Mironova, et al., Ross. Fiziol. Zh., 100, No. 12, 1409-1420 (2014).Google Scholar
  3. 3.
    N. E. Ordyan, I. V. Smolenskii, S. G. Pivina, and V. K. Akulova, Zh. Vyssh. Nervn. Deyat., 63, No. 2, 280 (2013).Google Scholar
  4. 4.
    S. G. Pivina, V. K. Akulova, V. V. Rakitskaya, and N. E. Ordyan, Bull. Exp. Biol. Med., 157, No. 3, 316-319 (2014).CrossRefPubMedGoogle Scholar
  5. 5.
    C. R. Bailey, E. Cordell, S. M. Sobin, and A. Neumeister, CNS Drugs, 27, No. 3, 221-232 (2013).CrossRefPubMedPubMedCentralGoogle Scholar
  6. 6.
    X. Belda, S. Fuentes, R. Nadal, and A. Armario, Horm. Behav., 54, No. 5, 654-661 (2008).CrossRefPubMedGoogle Scholar
  7. 7.
    J. D. Bremner, J. Licinio, A. Darnell, et al., Am. J. Psychiatry, 154, No. 5, 624-629 (1997).CrossRefPubMedPubMedCentralGoogle Scholar
  8. 8.
    N. P. Daskalakis, A. Lehrner, and R. Yehuda, Endocrinol. Metab. Clin. North Am., 42, No. 3, 503-513 (2013).CrossRefPubMedGoogle Scholar
  9. 9.
    B. S. McEwen, Dev. Neurobiol., 72, No. 6, 878-890 (2012).CrossRefPubMedPubMedCentralGoogle Scholar
  10. 10.
    V. Mironova, E. Rybnikova, and S. G. Pivina, Acta Physiol. Hung., 100, No. 4, 395-410 (2013).CrossRefPubMedGoogle Scholar
  11. 11.
    S. Yamamoto, S. Morinobu, S. Takei, et al., Depress. Anxiety, 26, No. 12, 1110-1117 (2009).CrossRefPubMedGoogle Scholar
  12. 12.
    R. Yehuda, Ann. N.Y. Acad. Sci., 1179, 56-59 (2009).CrossRefPubMedGoogle Scholar

Copyright information

© Springer Science+Business Media New York 2016

Authors and Affiliations

  • S. G. Pivina
    • 1
  • V. V. Rakitskaya
    • 1
  • V. K. Akulova
    • 1
  • N. E. Ordyan
    • 1
  1. 1.Laboratory of Neuroendocrinology, I. P. Pavlov Institute of PhysiologyRussian Academy of SciencesSt. PetersburgRussia

Personalised recommendations