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Therefore, circulating glucocorticoids can have contrasting effects in the amygdala and hippocampus, and these two structures can play contrasting roles in the activity of Bj rn otzik HPA axis. Converting errorcodes from COM objects to win32 errorcodes.!! Functional magnetic resonance imaging of facial affect recognition in children and adolescents. The amygdala is part of an extended neural network. Brain Behav. The amygdala is influenced by trauma of less intensity as well. Hippocampus 16—

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A Review of Adversity, The Amygdala and the Hippocampus: A Consideration of Developmental Timing

A review of the human developmental neuroimaging literature that investigates outcomes following exposure to psychosocial adversity is presented with a focus on two subcortical structures — the hippocampus and the amygdala.

Throughout this review, we discuss how a consideration of developmental timing of adverse experiences and age at measurement might provide insight into the seemingly discrepant findings across studies. We use findings from animal studies to suggest some mechanisms through which timing of experiences may result in differences across time and studies.

The literature suggests that early life may be a time of heightened susceptibility to environmental stressors, but that expression of these effects will vary by age at measurement.

Early adverse social environments such as abuse and neglect have been associated with a wide range of negative outcomes, including a dramatically increased risk for a variety of mental disorders Breslau et al.

These often include, but are not limited to, anxiety, depression, ADHD, substance use disorders, and tobacco dependence. The link between childhood trauma and adult risk for mental health disorders has been described in a variety of ways but fundamentally, this link is biological in nature.

These negative social environments become biologically embedded as changes in neural structure and function and, ultimately, the behaviors that lead to mental illness. Although initial susceptibilities for exposure to adversity may contribute to this association, pressures from the environment can alter neural development leading to negative outcomes.

Describing the mechanisms by which adverse experiences during childhood lead to changes in neural development is an important step for understanding both brain development and ultimately for developing tools for clinical intervention. In this review we will attempt to link the timing of negative childhood psychosocial stress exposure to differences in neural structure and function during childhood and adolescence.

We restrict this review to empirical articles that address psychosocial trauma of abuse and neglect. We further limit our review to the neural development of two subcortical structures: the hippocampus and amygdala. We focus on these two regions because, based on a large adult human and non-human animal literature, we would expect significant environmental influence on these structures.

The hippocampus and amygdala are important for socio-emotional functioning throughout development and are closely linked with the activity of the hypothalamic pituitary adrenocortical HPA axis, a significant neuroendocrine mediator of stressful events for humans. We purposefully narrow our focus to provide a richer discussion of the amygdala and hippocampus and how developmental timing interacts with environmental influences.

Because the systemic output of the HPA axis, glucocorticoids cortisol in humans , can pass through the blood-brain barrier, the HPA axis is one of the major pathways through which the effects of stress can shape brain development. The amygdala and hippocampus are rich with receptors for cortisol and are therefore major targets of the HPA axis. Thus, we see narrowing our review to the amygdala and hippocampus as one reasonable way to limit the scope of the neural effects of adversity that we examine here.

We will describe some specific examples of when amygdala and hippocampal development are disrupted by negative psychosocial environments.

By describing these associations, we hope to distill potential mechanisms by which exposure to adversity could become biologically embedded resulting in increased susceptibility to mental illness.

Finally we describe potential future directions for research. Throughout the review, we will be making the argument that the effects of adversity will vary as a function of developmental timing, such that regionally defined effects will depend on the age at which exposures occurred and when neural outcomes were measured. This focus on timing is consistent with the notion of sensitive periods identified in other developmental processes, such as vision or language, where developmental timing modifies the environment's impact on neural development.

A fundamental precept of developmental studies is that the timing of a particular exposure matters for the expression of a phenotype. Not all neural regions follow the same developmental trajectory Giedd et al. For example, primary sensory cortex such as V1 visual cortex appears to undergo important structural changes in the first year leading to life-long differences in visual perception, whereas other cortical regions e. In the case of binocular vision or phoneme perception, timing of environmental exposure and timing of measurement is critical for observation of normal perceptual development Hubel and Wiesel, ; Kuhl, These are powerful examples of the concept of a developmental sensitive period, which are periods of life when a system exhibits increased plasticity and therefore, susceptibility, to environmental influences.

Although the effects of sensitive periods are observed in behavior, they are properties of neural circuits see Knudsen, Central to this concept is the notion that the process of development itself may increase the system's likelihood of being shaped by the environment Casey et al. These periods often coincide with rapid development of a brain system, and therefore, individual neural systems will have their own sensitive periods Lupien et al.

Once environmental exposure occurs, it modifies the architecture of the circuit in such a way that certain patterns of future activity are preferred Knudsen, Therefore, knowing the developmental timing of environmental exposures is critical when evaluating its effects.

Beyond the timing of exposure, the timing of measurement can influence how we interpret the effects of environmental exposures, like adversity. Because compensatory neural mechanisms, which were not present during the stressor, may emerge once the adverse experience has terminated, timing should be well-characterized to disambiguate the effects of stress versus the effects of recovery.

Moreover, as will be discussed below, the effects of an environmental exposure may not emerge for some time after the termination of the exposure. In the case of adversity we predict that the timing of exposure i.

Psychosocial stress can adversely impact brain development, and the literature on stress suggests that these changes occur largely through the HPA axis reviewed in Loman and Gunnar, We will begin by briefly reviewing the structure of the HPA axis. A stressor sufficiently strong will elicit a full stress response Kemeny, which includes activation of both the sympathetic nervous system and activation of the HPA axis.

The latter, which produces a longer-term response to a stressor than the former hours rather than seconds to minutes , begins with signals from the amygdala reviewed in Herman and Cullinan, , which lead to peripheral systemic glucocorticoid increases via hypothalamus, pituitary, and adrenal gland activity and increases in corticotropin-releasing hormone in the brain CRH; including in the amygdala; Makino et al.

Eventually peripheral glucocorticoids make their way to the brain. Glucocorticoids easily pass through the blood-brain barrier Zarrow et al. When the stressor is removed and high circulating glucocorticoids are no longer necessary, glucocorticoids suppress HPA axis activation by occupying receptors in the hippocampus eventually inhibiting activity of the HPA axis van Haarst et al.

In contrast, glucocorticoid occupation of amygdala receptors can have a facilitating effect on the activity of the HPA axis, often increasing CRH production within the amygdala. Therefore, circulating glucocorticoids can have contrasting effects in the amygdala and hippocampus, and these two structures can play contrasting roles in the activity of the HPA axis.

As discussed in Gunnar and Quevedo , stress is a psychological condition in which the individual experiences challenges to their well-being that overwhelm their resources for coping.

Although this construct can be studied behaviorally and biologically Dantzer, , behavioral distress does not always mirror physiological stress reactions. However, elevated HPA axis activity can provide one biological index of stress, and importantly, one that can shape brain development. There is much evidence that children who are exposed to early adverse experiences, such as poverty Lupien et al.

Adverse caregiving is a type of stress also used in animal models. These models provide the opportunity, usually not available in humans, for examination of stress effects at the cellular level. A variety of stressors Bonaz and Rivest, , as well as administration of high levels of glucocorticoids Makino et al.

The amygdala has been understood to be functionally dormant in the rat neonatal period. In addition, CRH receptors are maximally expressed in the amygdala and hippocampus early in development reviewed in Baram and Hatalski, , a finding that may provide insight into why young animals are especially vulnerable to adversity. Moreover, high elevations of glucocorticoids can downregulate hippocampal receptors that normally aid in the negative feedback to the HPA axis van Haarst et al.

The process of glucocorticoids increasing hippocampal receptors occurs throughout development, including early in life Vazquez, We will discuss in greater detail below how the products of the HPA axis specifically affects both the hippocampus and the amygdala. The hippocampus has been implicated in learning and memory in adults and children.

In adults, when the hippocampus is removed surgically, encoding of long term memories is disrupted resulting in anterograde amnesia: new memories cannot be formed Markowitsch and Pritzel, Initial findings such as these in neuropsychological research were the result of bilateral hippocampal resection as a treatment for epilepsy including the famously described patient HM; Zola-Morgan et al. When the hippocampus is lesioned in children, a similar specific deficit in episodic memory is observed Vargha-Khadem et al.

As described above, in the context of stress exposure, the hippocampus has another important role; it provides a negative feedback mechanism, which modifies the HPA axis response as reviewed in Kim and Yoon, This negative feedback mechanism is accomplished via activation of glucocorticoid GR and mineralocorticoid receptors MR by circulating levels of glucocorticoids. At basal non-stress levels, the majority of MR are occupied by circulating levels of glucocorticoids.

During a typical HPA axis stress response, increased availability of glucocorticoids leads to GR occupation, activating a negative feedback loop and decreasing the HPA axis response. The immature ratio of MR to GR may result in unique hippocampal vulnerability to stress early in life.

As has been demonstrated in older animals, chronic occupation of GR may impair the hippocampally-mediated negative feedback process resulting in extended HPA axis activation following stressful events and dysregulation of the HPA axis. Down-regulation of hippocampal MR has been identified in very young rats as well reviewed in Vazquez, , which may increase the likelihood of GR occupation for young animals. In developmental neuroimaging studies, there is some evidence for age-related change increases in recruitment of the hippocampus during long-term memory tasks across late childhood Paz-Alonso et al.

Structural studies using magnetic resonance imaging MRI have revealed developmental differences in the volume of the hippocampus from birth through young adulthood. From birth to year 2, the hippocampus shows relatively little growth Knickmeyer et al. More substantial structural changes tend to be observed later in development.

In an initial cross-sectional study of children it was determined that the hippocampus showed protracted volumetric growth across childhood for girls but not boys Giedd et al. As will be discussed further below, the animal literature suggests that hippocampal development lags slightly behind amygdala development.

For example, whereas learning to pair a cue with a shock cued fear conditioning — an amygdala-dependent function is present by postnatal day 18 in the rat, the same aged rats are unable to pair a context to a shock contextual fear conditioning — a hippocampus dependent function; Rudy, These findings have been interpreted as occurring because of the relative immaturity of the hippocampus Cotman et al.

Despite the protracted development of the hippocampus, behavioral evidence suggests that some aspects of hippocampal function are present early in life. Across the first year of life, memory becomes increasingly context-independent, which is evidence of increased relational memory and involvement of the hippocampus Robinson and Pascalis, Extending putative hippocampal development into early childhood, Sluzenski and colleagues demonstrated that 4-year olds were not able to perform a relational memory task binding together pictures of animals and backgrounds whereas 6-year olds could and showed adult-like performance Sluzenski et al.

However, when using more familiar objects faces and scenes , 9-month-old infants showed evidence of intact relational memory Richmond and Nelson, Taken together, these findings are consistent with the notion that the basic relational function of the hippocampus is present early in life, although the hippocampus and its connections continue to show developmental change into adulthood.

Evidence from adult rodent models shows that stress exposure alters hippocampal volume and function in adulthood McEwen, , At baseline levels, glucocorticoids appear to aid memory formation by enhancing hippocampal excitability Diamond et al. However, during stress-induced HPA axis activation, hippocampal function is disrupted Diamond et al. Rodents exposed to early stress also demonstrate dendritic atrophy in hippocampal cells and decreased amplitude of long term potentiation in the CA3 area of the hippocampus, leading to deficits in memory formation Brunson et al.

Most animal studies of stress exposure examine pre- and early postnatal stress exposure or chronic stress exposure in the mature animal. To keep the parallels to human psychosocial trauma exposure as consistent as possible, we will not review the effects of prenatal stress here. Poor or absent maternal care has lasting effects on the hippocampus.

Early stress exposure of this variety is associated with decreased hippocampal volume and function and dysregulated HPA function in adulthood Liu et al. In one study of juvenile rodents, early exposure to chronic stress did not result in differences in the hippocampus h post stress but did 3-weeks post exposure when these rodents had reached adulthood Isgor et al.

In studies of mature rodents, chronic stress exposure is followed by hippocampal volume reductions h post stress exposure. Adult rodent stress exposure confers risk for short-term differences in hippocampal structure, which within ten stress-free days, reverse Conrad et al.

Intervention during the adolescent phase of development may modify the behavioral effects of juvenile stress exposures in rodents Francis et al. Thus, it appears that stress-related reductions in hippocampal volume and changes in HPA axis activation incurred as a result of juvenile stress exposure are more permanent than those incurred during adulthood Seckl and Meaney, In human adults, stress-related pathologies, such as major depressive disorder and post-traumatic stress disorder PTSD , correlate with decreased hippocampal volume Sheline et al.

Patients taking high doses of corticosteroids for long periods demonstrate hippocampally-mediated memory deficits Keenan et al. Finally, studies of adults who were exposed to abuse during childhood reveal decreases in hippocampal volume Bremner et al.

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