Prenatally stressed (PS) human infants and experimental animals show attentional deficits, hyperanxiety and disturbed social behavior. Impaired coping in stressful situations in adult PS monkeys and rodents is associated with dysregulation of the HPA axis, characterized by decreased feedback inhibition of corticotropin-releasing hormone (CRH) and prolonged elevation of plasma glucocorticoids in response to stress. PS rats have higher levels of CRH in the amygdala, fewer hippocampal glucocorticoid receptors and less endogenous opioid and GABA/BDZ (benzodiazepine) inhibitory activity. The mechanisms by which maternal stress induce these long-lasting changes in the developing fetal neuroaxis remain to be elucidated. It is suggested that impaired coping in stressful situations and dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, result from the action of maternal hormones released during stress on the developing fetus. The similarities in coping behavior and dysregulation of the HPA axis in PS animals to those in humans with depression, suggest that gestational stress, at a critical time during fetal development, may increase the propensity to develop this condition.