Brain Microglial Activation in Chronic Pain-Associated Affective Disorder

A growing body of evidence from both clinical and animal studies indicates that chronic neuropathic pain is associated with comorbid affective disorders. Spinal cord microglial activation is involved in nerve injury-induced pain hypersensitivity characterizing neuropathic pain. However, there is a l...

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Main Authors: Ellane Eda Barcelon, Woo-Hyun Cho, Sang Beom Jun, Sung Joong Lee
Format: Article
Language:English
Published: Frontiers Media S.A. 2019-03-01
Series:Frontiers in Neuroscience
Subjects:
Online Access:https://www.frontiersin.org/article/10.3389/fnins.2019.00213/full
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author Ellane Eda Barcelon
Woo-Hyun Cho
Sang Beom Jun
Sung Joong Lee
author_facet Ellane Eda Barcelon
Woo-Hyun Cho
Sang Beom Jun
Sung Joong Lee
author_sort Ellane Eda Barcelon
collection DOAJ
description A growing body of evidence from both clinical and animal studies indicates that chronic neuropathic pain is associated with comorbid affective disorders. Spinal cord microglial activation is involved in nerve injury-induced pain hypersensitivity characterizing neuropathic pain. However, there is a lack of thorough assessments of microglial activation in the brain after nerve injury. In the present study, we characterized microglial activation in brain sub-regions of CX3CR1GFP/+ mice after chronic constriction injury (CCI) of the sciatic nerve, including observations at delayed time points when affective brain dysfunctions such as depressive-like behaviors typically develop. Mice manifested chronic mechanical hypersensitivity immediately after CCI and developed depressive-like behaviors 8 weeks post-injury. Concurrently, significant increases of soma size and microglial cell number were observed in the medial prefrontal cortex (mPFC), hippocampus, and amygdala 8 weeks post-injury. Transcripts of CD11b, and TNF-α, genes associated with microglial activation or depressive-like behaviors, are correspondingly upregulated in these brain areas. Our results demonstrate that microglia are activated in specific brain sub-regions after CCI at delayed time points and imply that brain microglial activation plays a role in chronic pain-associated affective disorders.
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spelling doaj.art-d87f292da6354aaeacd9544127eab06d2022-12-22T02:25:11ZengFrontiers Media S.A.Frontiers in Neuroscience1662-453X2019-03-011310.3389/fnins.2019.00213439877Brain Microglial Activation in Chronic Pain-Associated Affective DisorderEllane Eda Barcelon0Woo-Hyun Cho1Sang Beom Jun2Sung Joong Lee3Department of Neuroscience and Physiology and Dental Research Institute, School of Dentistry, Seoul National University, Seoul, South KoreaDepartment of Neuroscience and Physiology and Dental Research Institute, School of Dentistry, Seoul National University, Seoul, South KoreaDepartment of Brain & Cognitive Sciences, Ewha Womans University, Seoul, South KoreaDepartment of Neuroscience and Physiology and Dental Research Institute, School of Dentistry, Seoul National University, Seoul, South KoreaA growing body of evidence from both clinical and animal studies indicates that chronic neuropathic pain is associated with comorbid affective disorders. Spinal cord microglial activation is involved in nerve injury-induced pain hypersensitivity characterizing neuropathic pain. However, there is a lack of thorough assessments of microglial activation in the brain after nerve injury. In the present study, we characterized microglial activation in brain sub-regions of CX3CR1GFP/+ mice after chronic constriction injury (CCI) of the sciatic nerve, including observations at delayed time points when affective brain dysfunctions such as depressive-like behaviors typically develop. Mice manifested chronic mechanical hypersensitivity immediately after CCI and developed depressive-like behaviors 8 weeks post-injury. Concurrently, significant increases of soma size and microglial cell number were observed in the medial prefrontal cortex (mPFC), hippocampus, and amygdala 8 weeks post-injury. Transcripts of CD11b, and TNF-α, genes associated with microglial activation or depressive-like behaviors, are correspondingly upregulated in these brain areas. Our results demonstrate that microglia are activated in specific brain sub-regions after CCI at delayed time points and imply that brain microglial activation plays a role in chronic pain-associated affective disorders.https://www.frontiersin.org/article/10.3389/fnins.2019.00213/fullbrain microgliamicroglial activationchronic paindepressionTNF-α
spellingShingle Ellane Eda Barcelon
Woo-Hyun Cho
Sang Beom Jun
Sung Joong Lee
Brain Microglial Activation in Chronic Pain-Associated Affective Disorder
Frontiers in Neuroscience
brain microglia
microglial activation
chronic pain
depression
TNF-α
title Brain Microglial Activation in Chronic Pain-Associated Affective Disorder
title_full Brain Microglial Activation in Chronic Pain-Associated Affective Disorder
title_fullStr Brain Microglial Activation in Chronic Pain-Associated Affective Disorder
title_full_unstemmed Brain Microglial Activation in Chronic Pain-Associated Affective Disorder
title_short Brain Microglial Activation in Chronic Pain-Associated Affective Disorder
title_sort brain microglial activation in chronic pain associated affective disorder
topic brain microglia
microglial activation
chronic pain
depression
TNF-α
url https://www.frontiersin.org/article/10.3389/fnins.2019.00213/full
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AT sungjoonglee brainmicroglialactivationinchronicpainassociatedaffectivedisorder