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Do maternal glucocorticoids transmit the programming effects of maternal stress to the fetus?

Research output: Contribution to conferencePoster

Original languageEnglish
Publication statusUnpublished - Jul 2018
EventParental Brain 2018: Biological and Behavioural Perspectives in Parental Health - Westin Harbour Castle Hotel, Toronto, Canada
Duration: 13 Jul 201814 Jul 2018
http://parentalbrain2018.com/

Conference

ConferenceParental Brain 2018
Abbreviated titlePB2018
CountryCanada
CityToronto
Period13/07/1814/07/18
Internet address

Abstract

Despite attenuated hypothalamo-pituitary-adrenal (HPA) axis responses to acute stress in pregnancy, chronic maternal stress exerts negative programming effects on the developing offspring. Here we investigated whether excess maternal glucocorticoid transfer to the fetus is the mechanism by which this occurs. Local concentrations of glucocorticoids are modulated by 11β-hydroxysteroid dehydrogenase (11βHSD) enzymes. In the brain, 11βHSD1 reactivates glucocorticoids, regulating glucocorticoid negative feedback of the HPA axis; whilst in the placenta, 11βHSD2 inactivates glucocorticoids, regulating glucocorticoid transfer across the maternal-fetal interface.
Pregnant rats were exposed to 10 min social stress/day from day 16 to 20 of pregnancy. Rats were killed following the final bout of stress and blood/tissues collected. Maternal plasma ACTH concentrations were measured by radioimmunoassay, while corticosterone concentrations were quantified using liquid chromatography-mass spectrometry. In situ hybridisation was performed to quantify mRNA expression for 11βHSD2 in the placenta and 11βHSD1 in the maternal brain and pituitary.
Plasma ACTH and corticosterone concentrations were significantly greater in the stressed dams compared with controls. Corticosterone concentrations were also significantly greater in both male and female placentae from stressed dams compared with controls. However, there was no significant effect of maternal stress on fetal plasma corticosterone concentrations in either sex. 11βHSD2 mRNA expression was greater in male, but not female placenta from stressed dams. In the maternal brain, social stress decreased 11βHSD1 mRNA expression in the paraventricular nucleus, dentate gyrus and CA3 of the hippocampus.
In conclusion, although repeated social stress activates the maternal HPA axis, the placental barrier appears intact and seemingly prevents maternal glucocorticoid transfer to the fetus. The data suggest maternal glucocorticoids are not directly involved in transmitting the programming effects of maternal stress to the foetuses. Whether indirect actions of maternal glucocorticoids are involved requires further investigation.

Event

Parental Brain 2018: Biological and Behavioural Perspectives in Parental Health

13/07/1814/07/18

Toronto, Canada

Event: Conference

ID: 68389420