Chronic maternal social stress is known exert negative programming effects in the developing foetus (Brunton and Russell, 2010). The mechanisms by which this occurs remains unclear, although a long-held hypothesis contends that excess maternal glucocorticoid transfer to the foetus may play a potential role (Seckl and Meaney, 2004). However, a “protective barrier” in the placenta exists, due to the presence of the enzyme 11βHSD2, which converts corticosterone (CORT) into the inactive metabolite 11-dehydrocorticosterone (11-DHC). 11βHSD2, together with 11βHSD1 (which catalyses the reverse reaction of reactivating CORT), is also expressed in other tissues such as the foetal brain, and both enzymes act in tandem to control local glucocorticoid concentrations. Here, we wanted to find out if maternal glucocorticoids are directly transferred from the maternal to foetal circulation following chronic maternal stress, and if the placental 11βHSD2 “protective barrier” may be compromised. Pregnant rats (n=7) were exposed to 10 min social stress each day from gestational day (GD) 16 to 20 via the modified resident-intruder paradigm. Rats were killed on GD20 immediately after the final stressor. CORT and 11-DHC concentrations in the maternal and foetal plasma, placenta, foetal brain and liver were quantified using liquid chromatography-mass spectrometry. In situhybridisation was also performed to quantify placental 11βHSD2 as well as glucocorticoid receptor (GR) mRNA expression, which may indicate placental glucocorticoid sensitivity. In the foetal hippocampus, mRNA expression of 11βHSD2 and 11βHSD1 was also investigated. Both plasma CORT and 11-DHC concentrations were dramatically increased in stressed pregnant dams compared to controls. Maternal stress significantly increased circulating CORT concentrations only in the female foetuses but not males, albeit to a smaller extent as compared to the maternal changes. CORT concentrations were significantly greater in the liver of both male and female foetuses following maternal stress; but no changes were detected in the foetal brain. 11-DHC concentrations were not different in foetal plasma nor brain/liver. In the placenta, stress resulted in elevated CORT concentrations and junctional zone 11βHSD2 mRNA expression only in males, but not females. There were no changes in placental GR mRNA expression, nor foetal hippocampal 11βHSD1 and 11βHSD2 mRNA expression in either sex. In conclusion, although repeated social stress increases the production of maternal CORT, the placental barrier appears intact, especially in the males, and the direct transfer of CORT from the maternal to foetal circulation is minimal. The data suggest maternal glucocorticoids are not directly involved in transmitting the programming effects of maternal stress to the foetuses, but may act in an indirect manner.