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Investigating the developmental sequelae of early life stress has provided researchers the opportunity to examine adaptive responses to extreme environments. A large body of work has established mechanisms by which the stressful experiences of childhood poverty, maltreatment, and institutional care can impact the brain and the distributed stress systems of the body. These mechanisms are reviewed briefly to lay the foundation upon which the current neuroimaging literature has been built. More recently, developmental cognitive neuroscientists have identified a number of the effects of early adversity, including differential behavior and brain function. Among the most consistent of these findings are differences in the processing of emotion and reward-related information. The neural correlates of emotion processing, particularly frontolimbic functional connectivity, have been well studied in early life stress samples with results indicating accelerated maturation following early adversity. Reward processing has received less attention, but here the evidence suggests a deficit in reward sensitivity. It is as yet unknown whether the accelerated maturation of emotion-regulation circuits comes at the cost of delayed development in other systems, most notably the reward system. This review addresses the early life stress neuroimaging literature that has investigated emotion and reward processing, identifying important next steps in the study of brain function following adversity. •Early life stress alters functional connectivity in emotion and reward circuits.•Early adversity may result in accelerated maturation of emotion processing systems.•Accelerated maturation of emotion processing may slow development of other systems.•Functional connectivity is a tool for studying psychopathology after early adversity.

This review provides a broad overview of my research group’s work on social buffering in human development in the context of the field. Much of the focus is on social buffering of the hypothalamic-pituitary-adrenocortical (HPA) system, one of the two major arms of the mammalian stress system. This focus reflects the centrality of the HPA system in research on social buffering in the fields of developmental psychobiology and developmental science. However, buffering of the cardiovascular and autonomic nervous system is also discussed. The central developmental question in this area derives from attachment theory, which argues that the infant’s experience of stress and arousal regulation in the context of her early attachment relationships is not an immature form of social buffering experienced in adulthood but rather the foundation out of which individual differences in the capacity to gain stress relief from social partners emerges. The emergence of social buffering in infancy, changes in social buffering throughout childhood and adolescence, the influence of early experience on later individual differences in social buffering, and critical gaps in our knowledge are described.

The handled-shocked and the handled-only group did equally well on every measure. [...]was born the research area known as infantile stimulation. An example of issues that the early rodent work highlighted that we should revisit but have not is the possibility that noxious stimulation has opposing effects at different points in development. [...]the same levels of shock that in preweaning rat pups results in less fearful behavior, when delivered to postweaning animals impairs functioning (Denenberg, 1964). All are associated with poor physical and psychological health with frequent or chronic activation of stress biology presumed to play a mediating role. Since the advent of developmental studies of adversity, psychologists have grappled with how to understand the relations between what children experience and how those experiences affect them. Because socialization was defined in this paper as parental emotion regulation, it is of course possible that genetic contributions to parent and child emotion regulatory abilities and not learning, per se, were the operative factors.

Research on the hypothalamic–pituitary–adrenocortical (HPA) axis has emerged as a vital area within the field of developmental psychopathology in the past 25 years. Extensive animal research has provided knowledge of the substrates and physiological mechanisms that guide development of stress reactivity and regulation using methods that are not feasible in humans. Recent advances in understanding the anatomy and physiology of the HPA axis in humans and its interactions with other stress-mediating systems, including accurate assessment of salivary cortisol, more sophisticated neuroimaging methods, and a variety of genetic analyses, have led to greater knowledge of how psychological and biological processes impact functioning. A growing body of research on HPA axis regulation and reactivity in relation to psychopathology has drawn increased focus on the prenatal period, infancy, and the pubertal transition as potentially sensitive periods of stress system development in children. Theories such as the allostatic load model have guided research by integrating multiple physiological systems and mechanisms by which stress can affect mental and physical health. However, almost none of the prominent theoretical models in stress physiology are truly developmental, and future work must incorporate how systems interact with the environment across the life span in normal and atypical development. Our theoretical advancement will depend on our ability to integrate biological and psychological models. Researchers are increasingly realizing the importance of communication across disciplinary boundaries in order to understand how experiences influence neurobehavioral development. It is important that knowledge gained over the past 25 years has been translated to prevention and treatment interventions, and we look forward to the dissemination of interventions that promote recovery from adversity.

Nonhuman animal models reveal that the hypothalamic–pituitary–adrenocortical (HPA) axis calibrates to the harshness of the environment during a sensitive period in infancy. Humans exposed to depriving institutional care in infancy show reduced HPA axis responsivity, even years after they are placed in supportive, well-resourced families. This study examined whether puberty opens a window of opportunity to recalibrate the HPA axis toward more typical reactivity when children shift from harsh deprived conditions in infancy into supportive conditions in childhood and adolescence. Participants (n = 129 postinstitutionalized, 68.2% female; n = 170 comparison, 52.4% female) completed 3 annual sessions beginning at ages 7 to 15 (M = 11.28, SD = 2.31). Each session assessed pubertal stage via nurse examination and cortisol reactivity to the Trier social stress test for children. The linear mixed-effects model controlling for sex and between-individual differences in pubertal stage showed a significant group by pubertal stage interaction: within-individual increases in pubertal stage were associated with increases in cortisol stress reactivity for postinstitutionalized youth but not nonadopted comparison youth. This study indicates that pubertal development reopens a window of opportunity for the HPA axis to recalibrate based on significant improvements in the supportiveness of the environment relative to that in infancy. The peripubertal period may be an important time in development where the caregiving environment has a substantial impact on the HPA axis and, perhaps, other stress-mediating systems. Future research is needed to examine the mechanisms of recalibration and whether HPA recalibration impacts physical and psychological health.

Key Points During stress there is activation of the hypothalamic-pituitary-adrenal (HPA) axis, culminating in the production of glucocorticoids. Glucocorticoids can easily access the brain, where they bind to receptors and influence the brain and behaviour. Different outcomes result from exposure to stress at different periods of an individual's life. Exposure to stress in the prenatal period leads to programming effects, as evidenced by increased reactivity to stress later in life and reduced hippocampal volume in adulthood. Exposure to prenatal stress has been associated with learning impairments, enhanced sensitivity to drugs of abuse, and increases in anxiety and depression-related behaviours in adulthood. Maternal separation is a potent stressor in the postnatal period, and it leads to increased secretion of glucocorticoids that can extend into adulthood. By contrast, exposure to severe abuse during infancy is associated with lower levels of glucocorticoids in both primates and humans. Stress during adolescence has more important effects on the HPA axis than a similar stress exposure during adulthood. Moreover, the effects of stress during adolescence can incubate until adulthood, at which time they will become apparent. The effects of stress exposure on the brain and behaviour in adulthood are similar to those that are observed in childhood and adolescence. However, unlike these latter effects, the former effects are reversible; that is, they usually disappear after cessation of the stressor. In adulthood, chronic exposure to high levels of glucocorticoids has been associated with depressive disorder. By contrast, patients with post-traumatic stress disorder present lower levels of glucocorticoids. The effects of stress during aging are associated with both memory impairments and reduced hippocampal volumes. The life cycle model of stress explains why different disorders emerge in populations exposed to stress at different stages of their lives. The effects of stress on the brain depend on the age at which the stress occurs. Reviewing data from animal and human studies, Lupien and colleagues discuss why different disorders emerge in individuals exposed to stress at different times in their lives. An interview with Sonia Lupien for Neuropod is available for download . Chronic exposure to stress hormones, whether it occurs during the prenatal period, infancy, childhood, adolescence, adulthood or aging, has an impact on brain structures involved in cognition and mental health. However, the specific effects on the brain, behaviour and cognition emerge as a function of the timing and the duration of the exposure, and some also depend on the interaction between gene effects and previous exposure to environmental adversity. Advances in animal and human studies have made it possible to synthesize these findings, and in this Review a model is developed to explain why different disorders emerge in individuals exposed to stress at different times in their lives.

The onset of adolescence, and more specifically the advent of pubertal maturation, represents a key developmental window for understanding the emergence of psychopathology in youth. The papers in this special section examine normative differences in the neurobiology of stress and emotional functioning over the peripubertal period. The work in this special section helps to fill in gaps in our understanding of key mechanisms that may contribute to increased vulnerabilities in behavioral and psychiatric morbidity during this developmental period.

Executive function (EF) abilities are increasingly recognized as an important protective factor for children experiencing adversity, promoting better stress and emotion regulation as well as social and academic adjustment. We provide evidence that early life adversity is associated with significant reductions in EF performance on a developmentally sensitive battery of laboratory EF tasks that measured cognitive flexibility, working memory, and inhibitory control. Animal models also suggest that early adversity has a negative impact on the development of prefrontal cortex-based cognitive functions. In this study, we report EF performance 1 y after adoption in 2.5- to 4-y-old children who had experienced institutional care in orphanages overseas compared with a group of age-matched nonadopted children. To our knowledge, this is the youngest age and the soonest after adoption that reduced EF performance has been shown using laboratory measures in this population. EF reductions in performance were significant above and beyond differences in intelligence quotient. Within the adopted sample, current EF was associated with measures of early deprivation after controlling for intelligence quotient, with less time spent in the birth family before placement in an institution and lower quality of physical/social care in institutions predicting poorer performance on the EF battery.

Home baseline and laboratory stressor (Trier Social Stress Test for Children) measures of salivary cortisol were obtained from 82 participants (40 girls) aged 9, 11, 13, and 15 years. Measures of pubertal development, self-reported stress, parent reports of child depressive symptoms and fearful temperament, and cardiac measures of sympathetic and parasympathetic activity were also obtained. Significant increases in the home cortisol baselines were found with age and pubertal development. Cortisol stress reactivity differed by age group with 11-year-olds and 13-year-old boys showing blunted reactivity and 9-year-olds, 13-year-old girls, and 15-year-olds showing significant cortisol reactions. Cortisol reactivity correlated marginally with sexual maturation. Measures of sympathetic activity revealed increased sympathetic modulation with age. Higher sympathetic tone was associated with more fearful temperament, whereas greater cortisol reactivity was associated with more anxious and depressed symptoms for girls. The importance of these findings for the hypothesis that puberty-associated increases in hypothalamic–pituitary–adrenal axis activity heightens the risk of psychopathology is discussed.