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Linking Mitochondria to Synapses: New Insights for Stress-Related Neuropsychiatric Disorders
The brain evolved cellular mechanisms for adapting synaptic function to energy supply. This is particularly evident when homeostasis is challenged by stress. Signaling loops between the mitochondria and synapses scale neuronal connectivity with bioenergetics capacity. A biphasic “inverted U shape” r...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4738951/ https://www.ncbi.nlm.nih.gov/pubmed/26885402 http://dx.doi.org/10.1155/2016/3985063 |
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author | Jeanneteau, Freddy Arango-Lievano, Margarita |
author_facet | Jeanneteau, Freddy Arango-Lievano, Margarita |
author_sort | Jeanneteau, Freddy |
collection | PubMed |
description | The brain evolved cellular mechanisms for adapting synaptic function to energy supply. This is particularly evident when homeostasis is challenged by stress. Signaling loops between the mitochondria and synapses scale neuronal connectivity with bioenergetics capacity. A biphasic “inverted U shape” response to the stress hormone glucocorticoids is demonstrated in mitochondria and at synapses, modulating neural plasticity and physiological responses. Low dose enhances neurotransmission, synaptic growth, mitochondrial functions, learning, and memory whereas chronic, higher doses produce inhibition of these functions. The range of physiological effects by stress and glucocorticoid depends on the dose, duration, and context at exposure. These criteria are met by neuronal activity and the circadian, stress-sensitive and ultradian, stress-insensitive modes of glucocorticoid secretion. A major hallmark of stress-related neuropsychiatric disorders is the disrupted glucocorticoid rhythms and tissue resistance to signaling with the glucocorticoid receptor (GR). GR resistance could result from the loss of context-dependent glucocorticoid signaling mediated by the downregulation of the activity-dependent neurotrophin BDNF. The coincidence of BDNF and GR signaling changes glucocorticoid signaling output with consequences on mitochondrial respiration efficiency, synaptic plasticity, and adaptive trajectories. |
format | Online Article Text |
id | pubmed-4738951 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-47389512016-02-16 Linking Mitochondria to Synapses: New Insights for Stress-Related Neuropsychiatric Disorders Jeanneteau, Freddy Arango-Lievano, Margarita Neural Plast Review Article The brain evolved cellular mechanisms for adapting synaptic function to energy supply. This is particularly evident when homeostasis is challenged by stress. Signaling loops between the mitochondria and synapses scale neuronal connectivity with bioenergetics capacity. A biphasic “inverted U shape” response to the stress hormone glucocorticoids is demonstrated in mitochondria and at synapses, modulating neural plasticity and physiological responses. Low dose enhances neurotransmission, synaptic growth, mitochondrial functions, learning, and memory whereas chronic, higher doses produce inhibition of these functions. The range of physiological effects by stress and glucocorticoid depends on the dose, duration, and context at exposure. These criteria are met by neuronal activity and the circadian, stress-sensitive and ultradian, stress-insensitive modes of glucocorticoid secretion. A major hallmark of stress-related neuropsychiatric disorders is the disrupted glucocorticoid rhythms and tissue resistance to signaling with the glucocorticoid receptor (GR). GR resistance could result from the loss of context-dependent glucocorticoid signaling mediated by the downregulation of the activity-dependent neurotrophin BDNF. The coincidence of BDNF and GR signaling changes glucocorticoid signaling output with consequences on mitochondrial respiration efficiency, synaptic plasticity, and adaptive trajectories. Hindawi Publishing Corporation 2016 2016-01-14 /pmc/articles/PMC4738951/ /pubmed/26885402 http://dx.doi.org/10.1155/2016/3985063 Text en Copyright © 2016 F. Jeanneteau and M. Arango-Lievano. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Jeanneteau, Freddy Arango-Lievano, Margarita Linking Mitochondria to Synapses: New Insights for Stress-Related Neuropsychiatric Disorders |
title | Linking Mitochondria to Synapses: New Insights for Stress-Related Neuropsychiatric Disorders |
title_full | Linking Mitochondria to Synapses: New Insights for Stress-Related Neuropsychiatric Disorders |
title_fullStr | Linking Mitochondria to Synapses: New Insights for Stress-Related Neuropsychiatric Disorders |
title_full_unstemmed | Linking Mitochondria to Synapses: New Insights for Stress-Related Neuropsychiatric Disorders |
title_short | Linking Mitochondria to Synapses: New Insights for Stress-Related Neuropsychiatric Disorders |
title_sort | linking mitochondria to synapses: new insights for stress-related neuropsychiatric disorders |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4738951/ https://www.ncbi.nlm.nih.gov/pubmed/26885402 http://dx.doi.org/10.1155/2016/3985063 |
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