It is perhaps obvious to hypothesize that the effects of exposure to elevations in glucocorticoid hormones in adolescence would differ from those in adulthood simply based on the fact of ongoing maturation of the HPA axis and of the CNS over adolescence. The system that is the basis of the reciprocal relationship between these hormones and the nervous system is the hypothalamic–pituitary–adrenal (HPA) axis. In turn, glucocorticoid hormones are under the regulation of the CNS. An important means by which this tuning is achieved is through shaping the development of the central nervous system (CNS) in early life and by moderating neural function and plasticity in adulthood. Another of their roles involves tuning the development of the organism in response to shifting demands of the environment. For example, they are involved in energy metabolism and coping responses to stressors, they influence immune and cardiovascular function, and they have several roles in mammalian pregnancy such as the maturation of fetal organs and the timing of parturition. Glucocorticoid hormones (primarily cortisol in people, corticosterone in rodents) affect the function of almost every cell type of the body (Dallman et al., 1987) and are important mediators of physical and physiological transitions in development (Wada, 2008). The effects of adolescent stress depend on a number of factors, including the age, gender, the duration of stress exposure, the type of stressor, and the time between stress exposure and testing.
Research progress in animal models in this field is reviewed including HPA function and the enduring effects of stress exposures in adolescence on sensitivity to drugs of abuse, learning and memory, and emotional behaviour in adulthood.
Although research on this period of life is scarce compared to early life and adulthood, the available research indicates that effects of stress exposure during adolescence differ from, and may be longer-lasting than, effects of the same stress exposure in adulthood. Developmental differences in hypothalamic–pituitary–adrenal (HPA) axis responsiveness to stressors and ongoing development of glucocorticoid-sensitive brain regions in adolescence suggest that similar to the neonatal period of ontogeny, adolescence may also be a sensitive period for programming effects of stressors on the central nervous system.