Chat with us, powered by LiveChat Developmental psych | Coms Paper
+1(978)310-4246 credencewriters@gmail.com
  

Write two short reading response on each of the article (75 words each)https://www.brighthorizons.com/family-resources/pa… and the one on the fileNeuroscience and Biobehavioral Reviews 34 (2010) 867–876
Contents lists available at ScienceDirect
Neuroscience and Biobehavioral Reviews
journal homepage: www.elsevier.com/locate/neubiorev
Review
Early experience and the development of stress reactivity and regulation
in children
Michelle M. Loman, Megan R. Gunnar *
The Early Experience, Stress, and Neurobehavioral Development Center1
Institute of Child Development, University of Minnesota, 51 East River Road, Minneapolis, MN 55455, USA
A R T I C L E I N F O
A B S T R A C T
Keywords:
Animal models
Caregiving
Child development
Deprivation
Emotion
Foster care
Institutional care
Regulation
Stress
Children who spend early portions of their lives in institutions or those maltreated in their families of
origin are at risk for developing emotional and behavioral problems reflecting disorders of emotion and
attention regulation. Animal models may help explicate the mechanisms producing these effects.
Despite the value of the animal models, many questions remain in using the animal data to guide studies
of human development. In 1999, the National Institute of Mental Health in the United States funded a
research network to address unresolved issues and enhance translation of basic animal early experience
research to application in child research. Professor Seymour Levine was both the inspiration for and an
active member of this research network until his death in October of 2007. This review pays tribute to his
legacy by outlining the conceptual model which is now guiding our research studies.
ß 2009 Elsevier Ltd. All rights reserved.
Contents
1.
2.
3.
4.
Conceptualizing early life stress . .
Early life stress model . . . . . . . . . .
2.1.
Stress-response system. . . .
2.2.
Threat-response system . . .
2.3.
Stress- and threat-response
2.4.
Development . . . . . . . . . . . .
2.5.
Caregiving . . . . . . . . . . . . . .
2.6.
Genetic processes . . . . . . . .
2.7.
Sex differences . . . . . . . . . .
Model in action . . . . . . . . . . . . . . .
Implications and future directions
Acknowledgements . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . .
……………………………..
……………………………..
……………………………..
……………………………..
systems: relations with PFC development .
……………………………..
……………………………..
……………………………..
……………………………..
……………………………..
……………………………..
……………………………..
……………………………..
* Corresponding author. Tel.: +1 612 624 2846; fax: +1 612 624 6373.
E-mail address: gunnar@umn.edu (M.R. Gunnar).
1
This NIMH Interdisciplinary Developmental Science Center members are
Jacqueline Bruce, Mary Dallman, Mary Dozier, Philip Fisher, Nathan Fox, Megan
Gunnar, Kai McCormack, Katherine Pears, Paul Plotsky, Seth Pollak, James Ritchie,
Mar Sanchez, and Stephen Suomi. Seymour Levine was a member of the research
network that gave rise to this NIMH Center. He passed away as we were in the
process of producing the grant revision that was funded.
0149-7634/$ – see front matter ß 2009 Elsevier Ltd. All rights reserved.
doi:10.1016/j.neubiorev.2009.05.007
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
868
869
869
870
870
871
871
872
872
872
873
874
874
Early life stress (ELS) in the form of adverse care from parents
and other caregivers increases the risk of psychopathology,
particularly disorders of emotion and attention regulation
(Kreppner et al., 2001; Provence and Lipton, 1962; Rogosch and
Cicchetti, 2005; Roy et al., 2004; Shields et al., 1994; Stevens et al.,
2008). While numerous studies document these increased risks,
we have only a limited understanding of the psychobiological
processes underlying them. Beginning with the pioneering work of
Seymour Levine (e.g. Levine, 1957), animal models have provided
868
M.M. Loman, M.R. Gunnar / Neuroscience and Biobehavioral Reviews 34 (2010) 867–876
insight into the mechanisms through which ELS alters the
development of stress- and threat-response systems (De Kloet
et al., 1988; Heim et al., 2004; Meaney and Szyf, 2005; Sanchez
et al., 2001). Animal models also provide evidence that alterations
in stress- and threat-response systems may compromise the
development of emotion- and attention-regulatory systems (Brake
et al., 2004; Vedhara et al., 2000). These animal data have often
been used to explain the heightened risk of behavioral and
affective disorders in human children exposed to ELS (e.g. Heim
and Nemeroff, 2001; Nemeroff, 2004). Nonetheless, the bridge
between the animal studies and human development is still more
hypothetical than empirically grounded (Bremner and Vermetten,
2001). Integration of the animal and human research requires a
conceptual model that is general enough to apply across species,
but specific enough to guide empirical investigations that allow
studies of children to inform animal models and in turn allow
animal model research to impact the design and interpretation of
human developmental research.
This paper describes the conceptual model developed by the
Early Experience, Stress, and Neurobehavioral Development
Research Network. This network is composed of basic researchers
studying the neurobiological processes involved in transducing the
effects of ELS in rodent and non-human primates, researchers
studying human development, and prevention science researchers
designing and examining early interventions. The work of first the
network, and now the Center, was inspired by Seymour (Gig)
Levine’s pioneering ‘‘early handling’’ research. Over the course of
over half a century, Dr. Levine established a rich body of research
on the role of early experience in the development of stress- and
threat-regulatory systems. From its inception, he interpreted his
animal model work as relevant to our understanding of human
development, particularly the development of depression and
anxiety disorders.
When the opportunity arose to establish an NIMH-network, Dr.
Levine was one of the first to champion the effort. At our first
meeting, he gave a tour-de-force lecture reviewing the history of
early experience stress research and noting how at each turn, new
methods gave opportunities to understand early experience effects
at more molecular levels of analysis, while also arguing that
developmental science, as a field, has continued to move between
describing early experiences as producing permanent (defining)
effects on development to describing them as being of little import,
being completely modifiable by later experiences. The tension
between these extreme positions became a common theme for our
network, and now our center, as we move forward to understand
both how ELS impact the developing organism and how best to
intervene to support optimal development for children exposed to
ELS during their earliest years.
1. Conceptualizing early life stress
There is no agreed upon definition of ELS; indeed, there is
considerable controversy about the definition of stress more
generally (Levine and Ursin, 1991). Our research network adopted
a working definition of ELS based on the following arguments.
Stressors are events or conditions that threaten, or are perceived to
threaten, physiological equilibrium (Weinstock, 2005). Stress
responses involve activity in the central nervous system to
mobilize endocrine, autonomic, and behavior systems to support
protection from and/or adaptation to threat. Recently the concept
of allostasis has been introduced to describe the dynamic
interaction of multiple systems of equilibrium maintenance
(McEwen, 1998, 2003). ELS or early life allostasis refers to
responses to stressors experienced during pre-pubertal development. While acknowledging that ELS can involve physical
stressors, we chose to focus on adverse caregiving in order to
ground our work in the early experience animal data. Furthermore,
we focused on stressors experienced during the first years of life
when the child is nearly wholly dependent on caregivers for its
survival.
Although the early experience animal data have been used to
explain the sequelae of childhood physical and sexual abuse (e.g.
Heim and Nemeroff, 2001), the animal models rest heavily on
the lack or loss of expectable parental care. These models more
closely approximate human conditions of deprivation and
neglect than those of physical or sexual abuse. However, while
animal models can be designed to focus on circumscribed types
of ELS, human ELS is messier. Studies of children in the child
welfare system, for example, note that it is rare to find children
exposed to only one type of maltreatment. Especially for
children under the age of five, physical and/or sexual abuse is
typically accompanied by neglect, with neglect constituting the
most frequent form of maltreatment for young children (chapter
5 in Barnett et al., 2005). Consistent with the human data, even
in non-human primates, physical abuse tends to co-occur with
high rates of maternal rejection and failure to protect the infant
(McCormack et al., 2006). Moreover, when both the frequency of
physical abuse and rejection are used to predict the lower levels
of CSF serotonin concentrations noted among abused Rhesus
infants, the results indicate that it is neglect/rejection that
predicts this neurobiological effect (Maestripieri et al., 2006a,b).
Among young children placed in foster care because of
maltreatment, markedly atypical cortisol diurnal rhythms are
associated with the child’s history of severe neglect, as
compared to physical or sexual abuse (Bruce et al., 2009a),
with similar findings noted for children living within the
markedly deprived conditions of an institution (e.g. orphanage;
Carlson and Earls, 1997). These findings, plus the prominence of
deprivation/disruption of parental care in the early experience
rodent models, led our network to focus on variations in the
amount and quality of parental care in conceptualizing ELS. This
is not to say that physical abuse or commission of harm does not
have an impact on development; however, these effects are
likely more related to trauma (see Yehuda and LeDoux, 2007).
Therefore, in our work on ELS, we have chosen to focus on the
loss or lack of typical parental care.
This focus is consistent with Levine’s (2005) argument that
lack or loss of species typical parental stimulation is among the
most potent stressors early in life. A focus on deprivation or loss
as a potent stressor is consistent with Hofer’s (1994) concept of
hidden regulators embedded in parent–offspring relationships.
He has argued that a number of sensorimotor, thermal, and
nutrient-based events that are components of typical parent–
offspring interactions have long-term regulatory effects on
specific components of infant behavior and physiology. Loss of
these hidden regulators results in wide-spread dysregulation of
physiological and behavioral responses during development
resulting in disturbances in circadian rhythms, growth (including brain growth factors, e.g. Cirulli et al., 2000) and hormone
levels (including activity of the hypothalamic–pituitary–adrenocortical [HPA] axis, e.g. Rosenfeld et al., 1992). Animal studies
also point to circuits involved in threat- and stress-system
functioning as particularly sensitive to disturbances in parental
nurturance (see review, Sanchez et al., 2001). Importantly,
though, recent rodent studies also indicate that later interventions may help ameliorate some (but not all) of the impact of
poor early nurturance (Bredy et al., 2003; Francis et al., 2002).
These findings along with our interest in translating basic
research to treatments led our network to give equal consideration to both the impacts of disturbances in early parental care
and possibility that improvement in care might support recovery
from ELS.
M.M. Loman, M.R. Gunnar / Neuroscience and Biobehavioral Reviews 34 (2010) 867–876
2. Early life stress model
As pictured in Fig. 1, this model notes that caregiving
experienced early in life regulates the activity of critical stresssensitive systems, which in turn influence the development of
systems involved in rapid appraisal and response to threat. Low
parental nurturance results in chronic stress to the infant. This
biases the developing threat system to rapidly orchestrate larger
defense responses (fight/flight/freeze). Overactivity of both stressand threat-response systems may then impact the development of
prefrontal regulatory systems, hence increasing the risk for both
attention- and emotion-regulatory problems. The neural systems
that orchestrate endocrine, autonomic, and behavioral rapid
defense responses are expected to be plastic during early childhood. If the child’s care improves, stress- and threat- systems have
the possibility to re-organize in order to become less reactive and
more modulated. However, children exposed to particularly severe
and prolonged inadequate nurturance may be less capable of reorganizing with improved care and this, in turn, may make it
difficult for caregivers to sustain appropriate responsiveness to the
child’s needs. One hypothesis is that re-organization of the stressand threat-response systems requires that the child experience
safety in his or her world. In early development, this requires that
the child develop a relationship with a consistently responsive,
caring adult. Therefore, this model also offers suggestions for
intervention efforts. Furthermore, while this model may apply to
most children (and to most developing mammals), vulnerability to
early adverse care and recovery in response to improved care are
Fig. 1. This represents the Center’s working model. It is purposely general enough to
apply to the various model systems (rodent, non-human primate, human) studied
by Center faculty. The model assumes that both genes and environment will
influence developing vulnerability to emotional and behavioral disorders. The
partially converging arrows running from left to right are meant to suggest
diminishing (but continuing) plasticity of the neurobiological systems underlying
risks for emotional and behavioral disorders. The facets of neurobiology depicted in
the model are the neurobiology of stress and the neurobiology of rapid threat
appraisal and response, along with developing behavioral and emotional regulatory
systems. Stress- and threat-response systems are depicted to the left within a larger
circle to indicate their earlier emergence in development. The circular arrows
connecting these two systems are meant to reflect their mutual influence on one
another. Emotional and behavioral regulatory systems reflect cortico-limbic
systems whose development is depicted to the right to indicate that it is
somewhat later developing. The circular arrows drawn between emotional and
behavioral regulatory systems and the circle containing the stress- and threatresponse systems indicate mutual influence across development. Finally, the aspect
of the environment most notable to our Center’s model is shown along the bottom
of the figure. This is the caregiving regulatory system. The spacing of the arrows is
designed to indicate that this system has more influence earlier in development, but
depending on the species, may continue to play a role well for prolonged periods of
the organism’s life.
869
expected to be influenced by the genetic differences among
individuals.
2.1. Stress-response system
As noted above, the biology of stress involves the interaction of
multiple systems of equilibrium maintenance (i.e. allostasis);
therefore, the box within Fig. 1 labeled ‘‘stress neurobiology’’ refers
conceptually to the multiple systems. However, for most of the
work relevant to this discussion, this box refers to activity of the
hypothalamic–pituitary–adrenocortical (HPA) axis and its neuroactive peptides and hormones. Note that the other major effector
arm of the mammalian stress-system is the sympatho-adrenal
system (Sapolsky et al., 2000). Although HPA activity is sometimes
measured solely as an index of stress, this neuroendocrine system
has multiple effects on brain development that make it an
attractive target for ELS research. Additionally, animal models that
form the basis of the preclinical information on ELS began with a
focus on the HPA system (see review, Levine, 2005). Glucorticoids
(GCs; cortisol in primates; corticosterone in rodents) are gene
transcription factors (i.e. influence gene expression; Meijer, 2006),
that can be measured non-invasively in young children. GCs are
permissive, their presence allowing or enhancing other neural,
molecular, or biochemical events. Acutely elevated GCs help to
terminate fight/flight physiological and behavioral responses.
However, when GCs and/or CRH remain elevated for prolonged
periods, this threatens neuronal viability and increases the risk of
stress-related disorders (De Kloet et al., 1996; McEwen, 2000).
GCs are produced by the adrenal cortex in response to
adrenocorticotropic hormone (ACTH) from the anterior pituitary.
Corticotropin-releasing hormone (CRH), produced by cells in the
hypothalamus, is the main stimulus of ACTH production.
Hypothalamic CRH, in turn, is regulated by neurocircuits conveying day/night information (i.e. diurnal rhythm of the HPA system)
and the state of the internal and external milieu (Herman and
Cullinan, 1997; Herman et al., 2002, 2005). Stressors (actual or
perceived threats) initiate a cascade beginning with hypothalamic
CRH release, increased pituitary ACTH secretion, and adrenal
production of GCs.
Throughout this discussion, we will sometimes use the
acronym L-HPA. The ‘‘L’’ in this case stands for limbic and conveys
the importance of limbic system in regulation of HPA responses to
psychological stressors (see review, Herman et al., 2005). Activation of the HPA axis to psychological stressors involves the
amygdala and perhaps the infralimbic cortex, while inhibition of
the HPA response involves the hippocampus and medial prefrontal
cortex (Diorio et al., 1993; Herman et al., 2005; Sullivan and
Gratton, 2002). These limbic sites have minimal direct projections
to CRH-producing regions in the hypothalamus. Instead, they relay
to these neurons via neurons in the bed nucleus of the stria
terminalis and regions in the hypothalamus and brainstem that
have access to hypothalamic CRH-producing neurons. The central
nucleus of the amygdala also has projections to brainstem regions
which activate sympatho-adrenal responses to stressors (Pitkanen
et…
Purchase answer to see full
attachment

error: Content is protected !!