Developmental consequences of prenatal administration of glucocorticoids in rodents and primates

Since their first use in 1972 by Liggins and Howie, prenatal exposure to synthetic glucocorticoids (GCs) is commonplace in antenatal medicine to impede the preterm birth-associated morbid symptoms. Synthetic GCs are ligands of the receptor of endogenous GC, the glucocorticoid receptor. Although prenatal GC is warranted for its increased survival rate of preterm infants, the repeated exposure to synthetic GC long-term effects has been questioned, and investigation of potentially harmful long-term effects in animal studies is required. I will first summarise the existing findings in animal studies, which include two robust phenotypes: A transient reduction of body weight and alteration of the hypothalamo-pituitary-adrenal gland axis activity. Several studies assessed the neurotransmitters' concentrations in animals exposed to prenatal GC and reported an overall increased activity of sero- toninergic and dopaminergic systems. Prenatal GC administration has also been shown to increase anxiety and reduce cognitive abilities in the long term. All these effects have been proposed to be mediated via epigenetics programming, which is the change of gene expression caused by mechanisms other than the DNA sequence (e.g. Promoter methylation). Interestingly, the same mechanism has been proposed to mediate the long-term effects of altered maternal behaviour, suggesting that the developing individual, from conception until weaning, is undergoing epigenetics programming based on its environment.