During critical or sensitive periods of development, the brain is highly plastic and particularly vulnerable to environmental adverse effects, including stress. In response to gestational stress, activation of the sympathetic system, the HPA axis and the central limbic stress loop increase the level of circulating glucocorticoids and catecholamines in both mother and foetus. Exposure to the excess amount of corticosteroids permanently reduces the glucocorticoid and mineralocorticoid receptors; thereby leading to an attenuation of the HPA axis feedback sensitivity and enhanced responsiveness to stress in the adult offspring. In the assessment of consequences at the behavioural, functional, and morphological levels; experimental animal models of maternal stress are extremely useful, in which the timing, intensity and duration of stress exposure can be readily controlled. These animal studies have revealed important links between prenatal stress exposure, life-long changes in the HPA function, and enhanced risk for subsequent psychopathology in a sex-specific manner. The aim of this review is to examine the impacts of prenatal stress on developmental anatomy of the brain, particularly focusing on the relevant emotional and behavioural outcomes within the context of current data obtained from experimental animals.
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