Exp Clin Endocrinol Diabetes 1991; 98(5): 123-129
DOI: 10.1055/s-0029-1211108
Original

© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Effect of an Acute Maternal Stress on the Fetal Hypothalamo-Pituitary-Adrenal System in Late Gestational Life of the Rat

Tomi Ohkawa, W. Rohde* , S. Takeshita, G. Dörner* , K. Arai, S. Okinaga
  • Department of Obstetrics and Gynecology, Teikyo University, School of Medicine, Tokyo/Japan
  • * Institute of Experimental Endocrinology, Humboldt University School of Medicine (Charité), Berlin/Germany
Further Information

Publication History

Publication Date:
16 July 2009 (online)

Summary

We investigated in this study the response of the fetal hypothalamo-pituitary-adrenal (HPA) system during an acute maternal stress in rats, in order to find out a possible role of developing fetal hypothalamus and to correlate its function to the androgen unbalance during the critical period of sex-specific brain differentiation. Pregnant rats of days 18 — 22 of gestation were subjected to an acute forced immobilization, and plasma levels of corticosterone (B) and ACTH were measured in mothers and fetuses. Hypothalamic contents of CRH and β-endorphin (EP), pituitary content of ACTH, and plasma levels of B and ACTH were measured in mothers and fetuses under the maternal stress on day 20 of gestation. By an acute exposure to the 20 minutes' stress, plasma levels of B and ACTH elevated significantly in mothers on each day of gestation. A significant increase of fetal plasma ACTH was detected from day 18 in males, and from day 20 in females. During the maternal stress on day 20 of gestation, hypothalamic contents of CRH and EP decreased significantly in male and female fetuses, when plasma levels of B and ACTH elevated significantly. These results indicate that fetal HPA axis seems to actually respond to the maternal stress during the late gestational period. Further, a release of CRH under the stress together with an activation of EP system in the fetal hypothalamus suggests a possible mechanism regulating the androgen secretion by the fetal hypothalamus via changes of the LH levels.