http://www.frontiersin.org/Journal/10.3389/fnbeh.2013.00158/full?utm_source=newsletter&utm_medium=email&utm_campaign=Neuroscience-w48-2013
Michael V. Baratta1*, Robert R. Rozeske2 and Steven F. Maier3
- 1Institute for Behavioral Genetics, University of Colorado Boulder, Boulder, CO, USA
- 2Neurocentre Magendie, INSERM U862, Bordeaux, France
- 3Department of Psychology and Neuroscience, University of Colorado Boulder, Boulder, CO, USA
Adverse events can impact brain structure and function
and are considered primary sources of risk for depression, anxiety, and
other psychiatric disorders. However, the majority of individuals who
encounter adverse or stressful life events do not develop untoward
outcomes, and so an understanding of the factors that promote resistance
to the deleterious effects of stress is of clinical importance. At the
level of basic research, there has been considerable effort directed at
identifying experimental parameters that blunt/augment outcomes from an
adverse event, but even when parameters are held constant, there is
inter-subject heterogeneity in behavior. This has shifted the focus to
understanding how genetic and experiential factors can shape an
organism's resistance to future adversity. The articles collected in the
present Research Topic provide an overview of recent efforts directed
at elucidating the neural mechanisms underlying resilience, and
utilizing such information to mitigate vulnerability.
Achieving genetic, epigenetic, and neural circuit-level
insight into the causal mechanisms underlying stress resilience has come
from a variety of disciplinary approaches. Wu et al. (2013)
lead this special issue by providing a comprehensive overview of recent
progress in each of these units of analysis. At the human level, much
of what is known about the biological determinants of resilience has
increasingly come from neuroimaging studies. In this issue van der Werff et al. (2013)
examine the structural and functional alterations related to
resilience, particularly contrasting findings of individuals who either
have, or have not, developed posttraumatic stress disorder (PTSD)
following trauma.
One of the consequences of long-term stress exposure is
to disrupt processes involved in successful adaptation to environmental
threat. The endogenous opioid peptide, β-endorphin, has been shown to
facilitate recovery following stress and here Barfield et al. (2013)
directly investigate its role in anxiety-like behaviors using
transgenic mice with varying capacities to synthesize the peptide. Vander Weele et al. (2013)
examine the contribution of another endogenous peptide, growth hormone
(GH), in hippocampal dysfunction following prolonged stress. The authors
demonstrate that chronic stress regimens reduce hippocampal GH and that
stress-induced hippocampal-dependent learning impairments are restored
following site-specific viral-mediated overexpression of GH. Their
findings implicate GH signaling in the hippocampus as a novel target for
promoting resilience following prolonged stress regimens.
Environmental conditions during development also
contribute to the heterogeneity of an individual's response to adversity
encountered as an adult. As Macrì (2013)
outlines, in an opinion piece, developmental conditions may be
harnessed to promote resilience in experimental settings. One such
experiential factor in humans, access to regular physical activity, has
long been known to positively modulate an individual's adaptive capacity
in the face of stress, an outcome that is readily observed with
voluntary wheel running in rodents (Greenwood and Fleshner, 2011). Here Loughridge et al. (2013)
combine laser capture microdissection with microarray expression
analysis to investigate novel molecular targets of exercise-induced
stress resistance. In addition to several genes that participate in
neural mechanisms previously shown to be critical in the impact of
exercise on stress, their innovative approach revealed sets of immune-
and circadian-related genes that deserve further investigation.
In many organisms, prior exposure to repeated stressors
often potentiates the neural and behavioral responses to later adverse
events, a phenomenon termed stress sensitization, which is thought to be
an important process involved in the susceptibility to anxiety
disorders. Conversely, a reduction in autonomic, neuroendocrine, and
behavioral responses is observed following repeated exposures to
identical stressors (homotypic stress), a phenomenon termed stress
habituation. Herman (2013)
discusses the mechanisms underlying habituation and the challenges of
identifying neural processes that represent a transition from adaptive
to maladaptive responding during conditions of chronic challenge.
Psychological and social factors (e.g., coping style,
cognitive flexibility, and social support) have long been associated
with resilience to adversity (Southwick et al., 2005),
although many of these factors are difficult to study in animals where
the underlying neural mechanisms can be directly explored. In an animal
model of intimate partner violence, Poirier et al. (2013)
examine the influence of baseline trait anxiety in female rats on the
neural and behavioral consequences of long-term cohabitation with an
aggressive male partner. Despite the fact that anxious temperament
modulated the behavioral outcome, many of the regional gene expression
patterns that are altered by cohabitation did not differ between the
“low” and “high” anxiety subgroups, highlighting the growing consensus
that mechanisms of resilience are not always the opposite of those
mediating vulnerability.
Additional psychosocial factors associated with resilience involve processes that engage coping strategies (Agaibi and Wilson, 2005).
Active coping is generally conceptualized as behavioral or
psychological efforts that individuals employ to master or reduce
negative circumstances. Actual or perceived behavioral control over some
aspect of the adverse event is central to coping, and Drugan et al. (2013)
provide a review of rodent paradigms in which the degree of behavioral
control is experimentally manipulated. The authors further discuss the
development of continuous non-invasive measurements (e.g., ultrasonic
vocalizations) within the original stress episode that may be predictive
of later performance during a subsequent challenge. On a related note, Nechvatal and Lyons (2013)
review how coping, within the context of stress exposure therapy,
impacts functional and structural measures in patients with specific
phobias or PTSD. A long-term goal of this line of research, the authors
note, is to guide the development of new intervention modalities that
enhance the neuroadaptations associated with coping with stress in order
to facilitate recovery.
Overall, the perspectives presented in this Frontiers in Behavioral Neuroscience
Research Topic represent an integrative approach for elucidating the
neural mechanisms underlying stress resilience. Extension of these
efforts to other experimental paradigms may identify common themes that
will very likely inform and enhance current therapeutic modalities.
References for their article at the link.
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