Prenatal Stress and Neurodevelopment of the Child: Focus on the HPA Axis and Role of the Placenta

• Published in: Developmental neuroscience Vol. 31; no. 4; pp. 285 - 292
• Main Authors: O’Donnell, K., O’Connor, T.G., Glover, V.
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland S. Karger AG 01.01.2009
• Subjects: 11-beta-Hydroxysteroid Dehydrogenase Type 2 - metabolism; Anxiety - complications; Child; Female; Humans; Hydrocortisone - blood; Hypothalamo-Hypophyseal System - physiology; Neurogenesis - physiology; Pituitary-Adrenal System - physiology; Placenta - metabolism; Pregnancy - psychology; Pregnancy Complications - etiology; Prenatal Exposure Delayed Effects; Stress; Stress, Psychological - complications; Stress, Psychological - physiopathology; Stress, Psychological - psychology; Neurodevelopment; Cortisol; Placenta; Fetal programming; 11-βHSD2; Prenatal stress
• ISBN: 3805592396; 9783805592390
• ISSN: 0378-5866; 1421-9859
• DOI: 10.1159/000216539

Recent human studies have shown that a wide variety of prenatal stressors, from anxiety and partner relationship problems, to natural disasters, increase the risk for a diverse range of adverse neurodevelopmental outcomes in the child. These include impaired cognitive development and behavioral problems, autism and schizophrenia. However, many questions remain about the underlying processes. Much of the research, based on animal studies, has focussed on the maternal HPA axis, with mixed results. Maternal stress or anxiety during pregnancy has been found to be weakly associated with raised maternal cortisol, if at all. The placenta may be a more promising programming vector, because it controls fetal exposure to the maternal environment. Animal studies indicate that prenatal stress can affect the activity of the placental barrier enzyme 11-βHSD2, which metabolises cortisol. We review the evidence for a similar mechanism in humans and how maternal stress may cause other changes in the placenta which affect fetal neurodevelopment.