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Putative Inflammatory Sensitive Mechanisms Underlying Risk or Resilience to Social Stress

It has been well recognized that exposure to stress can lead to the onset of psychosocial disorders such as depression. While there are a number of antidepressant therapies currently available and despite producing immediate neurochemical alterations, they require weeks of continuous use in order to...

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Autores principales: Finnell, Julie E., Wood, Susan K.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6212591/
https://www.ncbi.nlm.nih.gov/pubmed/30416436
http://dx.doi.org/10.3389/fnbeh.2018.00240
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author Finnell, Julie E.
Wood, Susan K.
author_facet Finnell, Julie E.
Wood, Susan K.
author_sort Finnell, Julie E.
collection PubMed
description It has been well recognized that exposure to stress can lead to the onset of psychosocial disorders such as depression. While there are a number of antidepressant therapies currently available and despite producing immediate neurochemical alterations, they require weeks of continuous use in order to exhibit antidepressant efficacy. Moreover, up to 30% of patients do not respond to typical antidepressants, suggesting that our understanding of the pathophysiology underlying stress-induced depression is still limited. In recent years inflammation has become a major focus in the study of depression as several clinical and preclinical studies have demonstrated that peripheral and central inflammatory mediators, including interleukin (IL)-1β, are elevated in depressed patients. Moreover, it has been suggested that inflammation and particularly neuroinflammation may be a direct and immediate link in the emergence of stress-induced depression due to the broad neural and glial effects that are elicited by proinflammatory cytokines. Importantly, individual differences in inflammatory reactivity may further explain why certain individuals exhibit differing susceptibility to the consequences of stress. In this review article, we discuss sources of individual differences such as age, sex and coping mechanisms that are likely sources of distinct changes in stress-induced neuroimmune factors and highlight putative sources of exaggerated neuroinflammation in susceptible individuals. Furthermore, we review the current literature of specific neural and glial mechanisms that are regulated by stress and inflammation including mitochondrial function, oxidative stress and mechanisms of glutamate excitotoxicity. Taken together, the impetus for this review is to move towards a better understanding of mechanisms regulated by inflammatory cytokines and chemokines that are capable of contributing to the emergence of depressive-like behaviors in susceptible individuals.
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spelling pubmed-62125912018-11-09 Putative Inflammatory Sensitive Mechanisms Underlying Risk or Resilience to Social Stress Finnell, Julie E. Wood, Susan K. Front Behav Neurosci Neuroscience It has been well recognized that exposure to stress can lead to the onset of psychosocial disorders such as depression. While there are a number of antidepressant therapies currently available and despite producing immediate neurochemical alterations, they require weeks of continuous use in order to exhibit antidepressant efficacy. Moreover, up to 30% of patients do not respond to typical antidepressants, suggesting that our understanding of the pathophysiology underlying stress-induced depression is still limited. In recent years inflammation has become a major focus in the study of depression as several clinical and preclinical studies have demonstrated that peripheral and central inflammatory mediators, including interleukin (IL)-1β, are elevated in depressed patients. Moreover, it has been suggested that inflammation and particularly neuroinflammation may be a direct and immediate link in the emergence of stress-induced depression due to the broad neural and glial effects that are elicited by proinflammatory cytokines. Importantly, individual differences in inflammatory reactivity may further explain why certain individuals exhibit differing susceptibility to the consequences of stress. In this review article, we discuss sources of individual differences such as age, sex and coping mechanisms that are likely sources of distinct changes in stress-induced neuroimmune factors and highlight putative sources of exaggerated neuroinflammation in susceptible individuals. Furthermore, we review the current literature of specific neural and glial mechanisms that are regulated by stress and inflammation including mitochondrial function, oxidative stress and mechanisms of glutamate excitotoxicity. Taken together, the impetus for this review is to move towards a better understanding of mechanisms regulated by inflammatory cytokines and chemokines that are capable of contributing to the emergence of depressive-like behaviors in susceptible individuals. Frontiers Media S.A. 2018-10-26 /pmc/articles/PMC6212591/ /pubmed/30416436 http://dx.doi.org/10.3389/fnbeh.2018.00240 Text en Copyright © 2018 Finnell and Wood. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Finnell, Julie E.
Wood, Susan K.
Putative Inflammatory Sensitive Mechanisms Underlying Risk or Resilience to Social Stress
title Putative Inflammatory Sensitive Mechanisms Underlying Risk or Resilience to Social Stress
title_full Putative Inflammatory Sensitive Mechanisms Underlying Risk or Resilience to Social Stress
title_fullStr Putative Inflammatory Sensitive Mechanisms Underlying Risk or Resilience to Social Stress
title_full_unstemmed Putative Inflammatory Sensitive Mechanisms Underlying Risk or Resilience to Social Stress
title_short Putative Inflammatory Sensitive Mechanisms Underlying Risk or Resilience to Social Stress
title_sort putative inflammatory sensitive mechanisms underlying risk or resilience to social stress
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6212591/
https://www.ncbi.nlm.nih.gov/pubmed/30416436
http://dx.doi.org/10.3389/fnbeh.2018.00240
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