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Early-life stress is a contributor to mental disorders across the
lifespan. Epidemiological studies have demonstrated that early-life
stress contributes not just to risk of mental disorders but
substantially to the risk of physical disease as well. It is also
clear that stress during early development has distinct effects upon
the nervous system when compared to trauma and stress experienced in
adulthood. Developmental stress has the capacity to program and
canalize the nervous system in ways that can profoundly alter how it
responds to future insults. These effects can be observed at
molecular, neuroanatomical, functional and behavioral levels. These
changes, mediated through alterations in neuroendocrine and
neuroimmune reactivity, can have complex and lasting consequences for
multiple organ systems that range beyond the brain to the gut and to
the cardiovascular system. Changes in cognition and behavior resulting
from early-life stress also contribute to social pathologies such as
delinquency, decreased school performance, and increased
incarceration. For these reasons, arriving at a mechanistic
understanding of how stress programs the brain in early life is a
first order concern with significant implications for public health,
public policy and neuroscience.
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This Research Topic will examine the many ways in which early-life
stress programs the brain and consequently the body across the
lifespan. Further, we will examine factors, which may prove protective
against early life stress. We will include contributions from
intersecting disciplines that seek to advance our understanding of how
early life stress changes the nervous system from basic science,
clinical and community perspectives.
Section 1: Introduction & Setup (CHARGE: Basic introduction,
but with a vague nod to the “allostatic curve and excitotoxicity”
model).
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Early life stress (ELS) is prevalent and is associated with multiple
hazards to development (namely heightened risk for many forms of
psychopathology
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The amygdala has been the focus of a great deal of attention in
research aimed at understanding the effects of early life stress.
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Essential functions of the amygdala
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A majority of past studies have shown increased amygdala activation to
social-emotional stimuli. Neural adaptation to chronic hyperactivity
has been termed allostasis and is associated with well-understood
changes in medial temporal lobe structures. Projecting cells of the
amygdala show increased dendritic volume and complexity in animal
models, which has been hypothesized to underlie the increased amygdala
volume after a single episode of depression in humans (McEwen, 2005).
Differences in dendritic complexity can account for differences in the
volume of regions in the amygdala (Cooke et al, 2007), so we expect
overall amygdala volume to parallel dendritic changes in the
allostatic load model. Since amygdala volume is decreased in chronic
depression, McEwen (2005) suggested that chronic overload might
eventually lead to amygdala atrophy. An important implication of this
model is that excitotoxic damage could eventually lead to cell death
in the amygdala at older ages. Consistent with this, the first
stereological study found decreased primary cell numbers in amygdalar
tissues from adults with autism (Schumann & Amaral, 2006).