Stress experienced by the mother while pregnant has consequences for the epigenome and behavior of her offspring. Exposure to maternal glucocorticoids is one potential mechanism by which maternal stress during gestation could induce damaging effects on offspring. In a study that employed restraint stress during pregnancy (day 14–20 of gestation), expression of 11β-hydroxysteroid dehydrogenase type 2 (Hsd11β2), which is important in protecting the developing fetus from circulating maternal glucocorticoids, was reduced in the placenta while DNA methylation of Hsd11β2 and Dnmt3a expression were increased (Pena et al., 2012). Dnmt1 expression was increased in the cortex of these animals (Pena et al., 2012), which could promote increased Hsd11β2 methylation. This effect has been replicated in humans, as higher self-reported stress during pregnancy was associated with increased methylation of HSD11B2 as well as FK506 Binding Protein 5 (FKBP5), a gene which has an inhibitory effect on glucocorticoid signaling, in the placenta (Monk et al., 2016). Further, increased methylation of both genes was linked with reduced fetal coupling (i.e. correlation between fetal movement and heart rate) (Monk et al., 2016). Reduced expression of
