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Microglia and Spinal Cord Synaptic Plasticity in Persistent Pain

Microglia are regarded as macrophages in the central nervous system (CNS) and play an important role in neuroinflammation in the CNS. Microglial activation has been strongly implicated in neurodegeneration in the brain. Increasing evidence also suggests an important role of spinal cord microglia in...

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Detalles Bibliográficos
Autores principales: Taves, Sarah, Berta, Temugin, Chen, Gang, Ji, Ru-Rong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3759269/
https://www.ncbi.nlm.nih.gov/pubmed/24024042
http://dx.doi.org/10.1155/2013/753656
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author Taves, Sarah
Berta, Temugin
Chen, Gang
Ji, Ru-Rong
author_facet Taves, Sarah
Berta, Temugin
Chen, Gang
Ji, Ru-Rong
author_sort Taves, Sarah
collection PubMed
description Microglia are regarded as macrophages in the central nervous system (CNS) and play an important role in neuroinflammation in the CNS. Microglial activation has been strongly implicated in neurodegeneration in the brain. Increasing evidence also suggests an important role of spinal cord microglia in the genesis of persistent pain, by releasing the proinflammatory cytokines tumor necrosis factor-alpha (TNFα), Interleukine-1beta (IL-1β), and brain derived neurotrophic factor (BDNF). In this review, we discuss the recent findings illustrating the importance of microglial mediators in regulating synaptic plasticity of the excitatory and inhibitory pain circuits in the spinal cord, leading to enhanced pain states. Insights into microglial-neuronal interactions in the spinal cord dorsal horn will not only further our understanding of neural plasticity but may also lead to novel therapeutics for chronic pain management.
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spelling pubmed-37592692013-09-10 Microglia and Spinal Cord Synaptic Plasticity in Persistent Pain Taves, Sarah Berta, Temugin Chen, Gang Ji, Ru-Rong Neural Plast Review Article Microglia are regarded as macrophages in the central nervous system (CNS) and play an important role in neuroinflammation in the CNS. Microglial activation has been strongly implicated in neurodegeneration in the brain. Increasing evidence also suggests an important role of spinal cord microglia in the genesis of persistent pain, by releasing the proinflammatory cytokines tumor necrosis factor-alpha (TNFα), Interleukine-1beta (IL-1β), and brain derived neurotrophic factor (BDNF). In this review, we discuss the recent findings illustrating the importance of microglial mediators in regulating synaptic plasticity of the excitatory and inhibitory pain circuits in the spinal cord, leading to enhanced pain states. Insights into microglial-neuronal interactions in the spinal cord dorsal horn will not only further our understanding of neural plasticity but may also lead to novel therapeutics for chronic pain management. Hindawi Publishing Corporation 2013 2013-08-18 /pmc/articles/PMC3759269/ /pubmed/24024042 http://dx.doi.org/10.1155/2013/753656 Text en Copyright © 2013 Sarah Taves et al. https://creativecommons.org/licenses/by/3.0/ 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
Taves, Sarah
Berta, Temugin
Chen, Gang
Ji, Ru-Rong
Microglia and Spinal Cord Synaptic Plasticity in Persistent Pain
title Microglia and Spinal Cord Synaptic Plasticity in Persistent Pain
title_full Microglia and Spinal Cord Synaptic Plasticity in Persistent Pain
title_fullStr Microglia and Spinal Cord Synaptic Plasticity in Persistent Pain
title_full_unstemmed Microglia and Spinal Cord Synaptic Plasticity in Persistent Pain
title_short Microglia and Spinal Cord Synaptic Plasticity in Persistent Pain
title_sort microglia and spinal cord synaptic plasticity in persistent pain
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3759269/
https://www.ncbi.nlm.nih.gov/pubmed/24024042
http://dx.doi.org/10.1155/2013/753656
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