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Structural plasticity of the adult brain: how animal models help us understand brain changes in depression and systemic disorders related to depression

The brain interprets experiences and translates them into behavioral and physiological responses. Stressful events are those which are threatening or, at the very least, unexpected and surprising, and the physiological and behavioral responses are intended to promote adaptation via a process called...

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Autor principal: McEwen, Bruce S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Les Laboratoires Servier 2004
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181799/
https://www.ncbi.nlm.nih.gov/pubmed/22034132
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description The brain interprets experiences and translates them into behavioral and physiological responses. Stressful events are those which are threatening or, at the very least, unexpected and surprising, and the physiological and behavioral responses are intended to promote adaptation via a process called “allostasis. ” Chemical mediators of allostasis include cortisol and adrenalin from the adrenal glands, other hormones, and neurotransmitters, the parasympathetic and sympathetic nervous systems, and cytokines and chemokines from the immune system. Two brain structures, the amygdala and hippocampus, play key roles in interpreting what is stressful and determining appropriate responses. The hippocampus, a key structure for memories of events and contexts, expresses receptors that enable it to respond to glucocorticoid hormones in the blood, it undergoes atrophy in a number of psychiatric disorders; it also responds to stressors with changes in excitability, decreased dendritic branching, and reduction in number of neurons in the dentate gyrus. The amygdala, which is important for “emotional memories, ” becomes hyperactive in posttraumatic stress disorder and depressive illness, in animal models of stress, there is evidence for growth and hypertrophy of nerve cells in the amygdala. Changes in the brain after acute and chronic stressors mirror the pattern seen in the metabolic, cardiovascular, and immune systems, that is, short-term adaptation (allostasis) followed by long-term damage (allostatic load), eg, atherosclerosis, fat deposition obesity, bone demineralization, and impaired immune function. Allostatic load of this kind is seen in major depressive illness and may also be expressed in other chronic anxiety and mood disorders.
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spelling pubmed-31817992011-10-27 Structural plasticity of the adult brain: how animal models help us understand brain changes in depression and systemic disorders related to depression McEwen, Bruce S. Dialogues Clin Neurosci State of the Art The brain interprets experiences and translates them into behavioral and physiological responses. Stressful events are those which are threatening or, at the very least, unexpected and surprising, and the physiological and behavioral responses are intended to promote adaptation via a process called “allostasis. ” Chemical mediators of allostasis include cortisol and adrenalin from the adrenal glands, other hormones, and neurotransmitters, the parasympathetic and sympathetic nervous systems, and cytokines and chemokines from the immune system. Two brain structures, the amygdala and hippocampus, play key roles in interpreting what is stressful and determining appropriate responses. The hippocampus, a key structure for memories of events and contexts, expresses receptors that enable it to respond to glucocorticoid hormones in the blood, it undergoes atrophy in a number of psychiatric disorders; it also responds to stressors with changes in excitability, decreased dendritic branching, and reduction in number of neurons in the dentate gyrus. The amygdala, which is important for “emotional memories, ” becomes hyperactive in posttraumatic stress disorder and depressive illness, in animal models of stress, there is evidence for growth and hypertrophy of nerve cells in the amygdala. Changes in the brain after acute and chronic stressors mirror the pattern seen in the metabolic, cardiovascular, and immune systems, that is, short-term adaptation (allostasis) followed by long-term damage (allostatic load), eg, atherosclerosis, fat deposition obesity, bone demineralization, and impaired immune function. Allostatic load of this kind is seen in major depressive illness and may also be expressed in other chronic anxiety and mood disorders. Les Laboratoires Servier 2004-06 /pmc/articles/PMC3181799/ /pubmed/22034132 Text en Copyright: © 2004 LLS http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle State of the Art
McEwen, Bruce S.
Structural plasticity of the adult brain: how animal models help us understand brain changes in depression and systemic disorders related to depression
title Structural plasticity of the adult brain: how animal models help us understand brain changes in depression and systemic disorders related to depression
title_full Structural plasticity of the adult brain: how animal models help us understand brain changes in depression and systemic disorders related to depression
title_fullStr Structural plasticity of the adult brain: how animal models help us understand brain changes in depression and systemic disorders related to depression
title_full_unstemmed Structural plasticity of the adult brain: how animal models help us understand brain changes in depression and systemic disorders related to depression
title_short Structural plasticity of the adult brain: how animal models help us understand brain changes in depression and systemic disorders related to depression
title_sort structural plasticity of the adult brain: how animal models help us understand brain changes in depression and systemic disorders related to depression
topic State of the Art
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181799/
https://www.ncbi.nlm.nih.gov/pubmed/22034132
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