Estes Y Plasticidad Cerebral

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Stress- and Allostasis-Induced Brain Plasticity
Bruce S. McEwen1 and Peter J. Gianaros2
1 Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University,New York, New York 10065; email: mcewen@mail.rockefeller.edu 2 Departments of Psychiatry and Psychology, University of Pittsburgh, Pittsburgh, Pennsylvania 15213

Annu. Rev. Med. 2011.62:431-445. Downloaded from www.annualreviews.org by Universidad de Antofagasta on 06/20/12. For personal use only.

Annu. Rev. Med. 2011. 62:431–45 First published online as a Review in Advance on August 10,2010 The Annual Review of Medicine is online at med.annualreviews.org This article’s doi: 10.1146/annurev-med-052209-100430 Copyright c 2011 by Annual Reviews. All rights reserved 0066-4219/11/0218-0431$20.00

Keywords
brain-body medicine, brain plasticity, hippocampus, amygdala, prefrontal cortex

Abstract
The brain is the key organ of stress processes. It determines what individuals willexperience 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. Theseallodynamic 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 ofbrain 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.

431

INTRODUCTION
Brain plasticity: the mutability of brain structure and function as a result of experience

Annu. Rev. Med. 2011.62:431-445. Downloaded fromwww.annualreviews.org by Universidad de Antofagasta on 06/20/12. For personal use only.

Stress and stressful experiences have long been implicated in the etiology and pathophysiology of chronic physical and mental health conditions that now pose a great threat to public health (1). Historically, disciplinary variation in defining and studying stress and stressful experiences posed both methodological andconceptual challenges to the medical community’s understanding of how an individual’s health status could be affected by such complex processes over the life course. These challenges have been addressed by current perspectives, which build on recent advances in translational animal and human research and emphasize that the relationships between stressful experiences and health status depend on adynamic interaction between genetic liability and exposure to environmental factors. This interaction begins in utero and continues until death (2). Canonically, we can label a stressful experience as “good,” “tolerable,” or “toxic” depending on the extent to which an individual has control over a given stressor and has support systems and resources in place for coping with it (3, 4). Meeting thedemands imposed by stressful experiences can lead to growth, adaptation,

and beneficial forms of learning that promote resiliency and good health. By contrast, other stressful experiences can foster a proliferation of recursive neural, physiological, behavioral, cognitive, and emotional changes that increase vulnerability to ill health and premature death by several chronic medical conditions...
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