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Horm Metab Res 2005; 37(3): 172-177
DOI: 10.1055/s-2005-861303
Original Clinical
© Georg Thieme Verlag KG Stuttgart · New York

Three-generation Investigation on Serotonin Content in Rat Immune Cells long after β-endorphin Exposure in Late Pregnancy

G.  Csaba1 , C.  Karabélyos2 , Á.  Inczefi-Gonda1 , É.  Pállinger3
  • 1Department of Genetics, Cell and Immunobiology, Semmelweis University, Budapest
  • 2Biotest Hungaria Ltd. Budapest
  • 3Molecular Immunological Research Group, Hungarian Academy of Sciences, Budapest
Further Information

Publication History

Received 19 July 2004

Accepted after revision 1 September 2004

Publication Date:
12 April 2005 (online)

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Abstract

Female rats were treated with β-endorphin on the 19th day of pregnancy. Serotonin content of immune cells (peritoneal lymphocytes, monocyte-macrophage-granulocyte group (mo-gran), mast cells, blood lymphocytes, granulocytes and monocytes, thymus lymphocytes) were studied in the mothers (P-generation four weeks after delivery), in the male offspring (F1) generation (at seven weeks), in the female offspring (four weeks after their own delivery) and in their offspring (F2 generation, at seven weeks). P-mother cells’ serotonin content was not influenced by endorphin treatment, while F1 generation’s mo-gran and blood lymphocyte serotonin content was reduced (in contrast, histamine content of mo-gran increased). Four weeks after delivery, an increase in serotonin content was observed in the F1 generation in the peritoneal lymphocytes and mast cells as well as in blood lymphocytes. In contrast, serotonin content was reduced in blood granulocytes and monocytes. In the F2 (grandson) generation, a reduction in mast cell serotonin content and sensitization of blood and thymic lymphocytes to repeated endorphin treatment was provoked. The significant changes were more expressed in the F2 generation compared to F1, also appearing earlier. The results unequivocally suggest that the increase in endorphin levels during late pregnancy can cause permanent changes in the F1 and F2 generations, which means that the imprinting effect can be transgenerationally transmitted.

Key words

Transgenerational effect - Serotonin - Endorphin - White blood cells - Mast cells - Hormonal imprinting

References

  • 1 Csaba G. The present state in the phylogeny and ontogeny of hormone receptors.  Horm Metab Res. 1984;  16 329-335
    PubMedGoogle Scholar
  • 2 Csaba G. Receptor ontogeny and hormonal imprinting.  Experientia. 1986;  42 750-759
    PubMedGoogle Scholar
  • 3 Csaba G. Phylogeny and ontogeny of chemical signaling: origin and development of hormone receptors.  Internat Rev Cytol. 1994;  155 1-48
    PubMedGoogle Scholar
  • 4 Csaba G. Hormonal imprinting: its role during the evolution and development of hormones and receptors.  Cell Biol Int. 2000;  24 407-414
    CrossrefPubMedGoogle Scholar
  • 5 Bern H A, Gorski R A, Kawashima S. Long term effects of prenatal hormone administration.  Science. 1973;  181 189-190
    PubMedGoogle Scholar
  • 6 Bern H A, Jones L A, Mori T, Young P N. Exposure of neonatal mice to steroids: long term effects on the mammary gland and other reproductive structures.  J Ster Biochem. 1975;  6 673-676
    PubMedGoogle Scholar
  • 7 Tchernitchin A, Tchernitchin N. Imprinting of paths of heterodifferentiation by prenatal or neonatal exposure to hormones, pharmaceuticals, pollutants and other agents and conditions.  Med Sci Res. 1992;  20 391-397
    PubMedGoogle Scholar
  • 8 Csaba G, Kovács P, Pállinger E. Single treatment (hormonal imprinting) of newborn rats with serotonin increases the serotonin content of cells in adults.  Cell Biol Int. 2002;  26 663-668
    CrossrefPubMedGoogle Scholar
  • 9 Csaba G, Inczefi-Gonda A. Effect of late steroid imprinting of the thymus on the hormone binding capacity of thymocytic receptors in adulthood.  Acta Physiol Hung. 1990;  15 195-199
    PubMedGoogle Scholar
  • 10 Csaba G, Kovács P, Pállinger E. Effect of endorphin exposure at weaning on the endorphin and serotonin content of white blood cells and mast cells in adult rat.  Cell Biochem Function. 2004;  22 197-200
    PubMedGoogle Scholar
  • 11 Csaba G, Kovács P, Pállinger E. Effect of a single neonatal endorphin treatment on the hormone content of adult rat white blood cells and mast cells.  Cell Biol Int. 2003;  27 423-427
    CrossrefPubMedGoogle Scholar
  • 12 Csaba G, Knippel B, Karabélyos C, Inczefi-Gonda A, Hantos M, Tóthfalusi L, Tekes K. Effect of neonatal β-endorphin imprinting on sexual behavior and brain serotonin level in adult rats.  Life Sci. 2003;  73 103-114
    CrossrefPubMedGoogle Scholar
  • 13 McPherson G A. Analysis of radioligand binding experiments and microcomputing system.  Trends Biochem Sci. 1983;  41 369-370
    PubMedGoogle Scholar
  • 14 McPherson G A. Analysis of radioligand binding experiments: a collection of computer programs to the IBM PC.  J Pharmacol Meth. 1985;  14 213-218
    CrossrefPubMedGoogle Scholar
  • 15 Madlafousek J, Hlinak Z. Sexual behavior of female laboratory rat: inventory, patterning and measurement.  Behavior. 1977;  63 29-174
    PubMedGoogle Scholar
  • 16 Gianoulakis C. Effect of maternally administered opiates on the development of the beta-endorphin system in the offspring.  NIDA Res Monogr. 1986;  75 595-598
    PubMedGoogle Scholar
  • 17 Insel T R, Kinsley C H, Mann P E, Bridges R S. Prenatal stress has long-term effects on brain opiate receptors.  Brain Res. 1990;  511 93-97
    CrossrefPubMedGoogle Scholar
  • 18 Sternberg W F, Ridgway C G. Effects of gestational stress and neonatal handling on pain, analgesia and stress behavior of adult mice.  Physiol Behav. 2003;  78 375-383
    CrossrefPubMedGoogle Scholar
  • 19 Campbell J H, Perkins P. Transgenerational effects of drug and hormonal treatments in mammals: a review of observations and ideas.  Progr Brain Res. 1988;  73 535-553
    PubMedGoogle Scholar
  • 20 Kaati G, Bygren L O, Edvinsson S. Cardiovascular and diabetes mortality determined by nutrition during parents’ and grandparents’ slow growth period.  Eur J Human Genet. 2002;  10 682-688
    CrossrefPubMedGoogle Scholar
  • 21 Mossberg H O. 40-year follow-up of overweight children.  Lancet. 1989;  2 491-493
    PubMedGoogle Scholar
  • 22 Diamond J. War babies. In:Ceci S, Williams W (eds) The nature-nurture debate. Blackwell; Oxford 2000: 14-22
    Google Scholar
  • 23 Holliday R. DNA methylation and epigenetic inheritance.  Philos Trans R Soc Lond B. 1990;  326 329-338
    PubMedGoogle Scholar
  • 24 Reik W, Dean W, Walter J. Epigenetic reprogramming in mammalian development.  Science. 2001;  293 1089-1093
    CrossrefPubMedGoogle Scholar
  • 25 Roemer I, Reik W, Dean W, Klose J. Epigenetic inheritance in the mouse.  Curr Biol. 1997;  7 277-280
    CrossrefPubMedGoogle Scholar
  • 26 Monk M. Epigenetic programming of differential gene expression in development and evolution.  Dev Genet. 1995;  17 188-197
    CrossrefPubMedGoogle Scholar
  • 27 Barraclough C A, Gorski R A. Studies on mating behavior in the androgen sterilized female rat in relation to the hypothalamic regulation of sexual behavior.  J Endocrinol. 1962;  25 175-182
    PubMedGoogle Scholar
  • 28 Csaba G, Knippel B, Karabélyos C, Inczefi-Gonda A, Hantos M, Tekes K. Endorphin excess at weaning durably influences sexual activity, uterine estrogen receptor’s binding capacity and brain serotonin level of female rats.  Horm Metab Res. 2004;  36 39-43
    Article in Thieme ConnectPubMedGoogle Scholar
  • 29 Barkan T, Gurwitz D, Lavy G, Weizman A, Rehavi M. Biochemical and pharmacological characterization of the serotonin transporter in human peripheral blood lymphocytes.  Eur Neuropsychopharmacol. 2004;  14 237-243
    CrossrefPubMedGoogle Scholar
  • 30 Sugimoto Y, Inoue K, Yamada J. Involvement of 5-HT2 receptor in imipramine-induced hyperglycemia in mice.  Horm Metab Res. 2003;  35 511-516
    Article in Thieme ConnectPubMedGoogle Scholar
  • 31 Mossner R, Lesch K P. Role of serotonin in the immune system and in neuroimmune interactions.  Brain Behav Immun. 1998;  12 249-271
    CrossrefPubMedGoogle Scholar

Prof. G. CsabaMD, PhD 

Semmelweis University of Medicine · Department of Genetics, Cell and Immunobiology

POB 370 · H-1445 Budapest · Hungary

Phone: +36(1)2102950

Fax: +36(1)2102950 ·

Email: csagyor@dgci.sote.hu