Stress- and Allostasis-Induced Brain Plasticity

By Bruce S. McEwen, Peter J. Gianaros. Annual Review of Medicine, 2011

1,089 citations recorded by the source corpus.

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.

Subfields: Behavioral Neuroscience, Developmental Neuroscience, Physiology

View Paper: https://www.semanticscholar.org/paper/b8926f1c290a3f3f9fc57e4b74ae4393f3b9ddf3

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Citations in the corpus

The Neuroendocrinology of Social Isolation (2014, background): “Glucocorticoids are small, lipophilic molecules that cross the blood-brain barrier, where they are involved in a number of processes including neuronal cell birth, differentiation, apoptosis, dendritic arborization, and synaptic function (McEwen & Gianaros 2011, Riedemann et al. 2010).”
More than a feeling: A unified view of stress measurement for population science (2018, background): “This latter finding is important because the hippocampus is replete with glucocorticoid receptors and thus renders the hippocampus at risk for atrophy when exposed to the high doses of glucocorticoids observed in response to prolonged stress in animal models (McEwen, 1999; Sapolsky, 1999), as well a”
Sex Differences in Stress-Related Psychiatric Disorders: Neurobiological Perspectives (2014, background): “These glucocorticoids then “feedback” on glucocorticoid receptors (GRs) in the PVN and pituitary to limit activation of this system [35; 36; 37].”
Brain on stress: How the social environment gets under the skin (2012, background): “, interventions that involve integrated CNS activity as opposed to pharmacological agents) that include cognitive behavioral therapy, physical activity, and programs that promote social support and integration and meaning and purpose in life (2, 3, 95).”
Brain On Stress: Vulnerability and Plasticity of the Prefrontal Cortex Over the Life Course (2013, neutral): “…depression, and PTSD (Arnsten, 2009a; Drevets et al., 1997b; Gamo and Arnsten, 2011; Tan et al., 2007), and it is also vulnerable to stress (McEwen and Gianaros, 2011) and normal aging (Morrison and Baxter, 2012), as well as Alzheimer's disease (Hof and Morrison, 2004; Morrison and Hof,…”
Modulating prefrontal cortex activity to alleviate stress-induced working memory deficits: A transcranial direct current (tDCS) study (2024, unknown): “Stress in classical terms is defined as a state of increased allostatic load resulting from exposure to various triggers, leading to a feeling of loss of control over physiological and psychological responses (McEwen & Gianaros, 2011).”