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Stress- and Allostasis-Induced Brain Plasticity
Open accessAbstract
The brain is the key organ of stress processes. It determines what individuals will experience as stressful, it orchestrates how individuals will cope with stressful experiences, and it changes both functionally and structurally as a result of stressful experiences. Within the brain, a distributed, dynamic, and plastic neural circuitry coordinates, monitors, and calibrates behavioral and physiological stress response systems to meet the demands imposed by particular stressors. These allodynamic processes can be adaptive in the short term (allostasis) and maladaptive in the long term (allostatic load). Critically, these processes involve bidirectional signaling between the brain and body. Consequently, allostasis and allostatic load can jointly affect vulnerability to brain-dependent and stress-related mental and physical health conditions. This review focuses on the role of brain plasticity in adaptation to, and pathophysiology resulting from, stressful experiences. It also considers interventions to prevent and treat chronic and prevalent health conditions via allodynamic brain mechanisms.
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“environmental conditions and interpersonal interactions, both positive and negative, are embedded biologically, shaping or canalizing the development of brain and behavior”
From School Readiness and Self-Regulation: A Developmental Psychobiological Approach (2015) · cites this paper as McEwen & Gianaros 2011
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“Extensive literature links ELA to pervasive, quantifiable variation in brain structure and function [15, 21, 24, 25].”
From Biological embedding of childhood adversity: from physiological mechanisms to clinical implications (2017) · cites this paper as [15]
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“Importantly, HPA hyper- and hypo-reactivity both represent prototypical patterns associated with excess allostatic load, and both predict human stress-related chronic illnesses, including cardiovascular, metabolic, and psychiatric diseases linked epidemiologically to ELA [15, 29, 48].”
From Biological embedding of childhood adversity: from physiological mechanisms to clinical implications (2017) · cites this paper as [15]
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“Such an approach facilitates the synthesis of complex evidence for application, and is supported by observed dose–response effects linking cumulative early adversity to later outcomes [1, 3, 5], and by the “allostatic load” paradigm exploring pathogenic effects of cumulative all-cause stress [15].”
From Biological embedding of childhood adversity: from physiological mechanisms to clinical implications (2017) · cites this paper as [15]
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“However, chronic or excessive activation contributes to the pathogenic physiological “wear and tear” described within the allostatic load paradigm [15, 29].”
From Biological embedding of childhood adversity: from physiological mechanisms to clinical implications (2017) · cites this paper as [15]
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“These experience-dependent mechanisms regulate the sensitivity and plasticity of the central nervous system and act at several biological levels (likely partly in parallel with each other): i) cellular changes such as neurogenesis, pruning and sprouting of synapses, myelination of axons and alterations to the number of dendritic spines9, 10, ii) subcellular changes, such as alterations to the”
From Resilience in mental health: linking psychological and neurobiological perspectives. (2013) · cites this paper as [9]
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“The shape of the inverted U differs by many factors including sex, strain, and behavioral domain in question (Fig. 2).”
From Neurobiology of resilience (2012) · cites this paper as [50]
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“McEwen and colleagues systematically measured the type, length, and quality of stress experience on multiple rat behaviors and found that stress affects most behavioral domains with an inverted U–shape curve, where low and high levels of stress both impair behavior, while intermediate levels actually promote positive coping responses (for review see50).”
From Neurobiology of resilience (2012) · cites this paper as [50]
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Metadata
- Authors
- McEwen, B. S., & Gianaros, P. J.
- Affiliations
- Rockefeller University (US)
- University of Pittsburgh (US)
- Venue
- Annual Review of Medicine
- Publisher
- Annual Reviews
- Published
- 2011-02-18
- Volume
- 62
- Issue
- 1
- Pages
- 431-445
- ISSN
- 0066-4219 (ISSN-L)
- 1545-326X
- PMC
- PMC4251716
- OpenAlex
- W2116769635
- Cited by
- 1,171
- References
- 74
- Citations by year
- 2026: 96 · 2025: 100 · 2024: 78 · 2023: 55 · 2022: 98 · 2021: 81 · 2020: 81 · 2019: 86 · 2018: 60 · 2017: 83 · 2016: 79 · 2015: 64 · 2014: 73 · 2013: 54 · 2012: 58
- FWCI
- 3.81
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annual Review of Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Heart, Lung, and Blood Institute (R01HL089850)
- National Institute of Mental Health (5P01 MH58911, K01MH070616, R01 MH41256, P50MH058911, R01MH041256)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Social Sciences › Psychology › Clinical Psychology › Child Abuse and Trauma
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- allostasis, allostatic load, neuroplasticity, stress response, stress-related disorders, stress adaptation, stress coping
- MeSH terms
- Adaptation, Physiological, Adaptation, Psychological, Animals, Brain, Female, Humans, Male, Neuronal Plasticity, Stress, Physiological, Stress, Psychological, Mice, Rats, Allostasis
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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