Cargando…

Neuronal-Glial Interactions Maintain Chronic Neuropathic Pain after Spinal Cord Injury

The hyperactive state of sensory neurons in the spinal cord enhances pain transmission. Spinal glial cells have also been implicated in enhanced excitability of spinal dorsal horn neurons, resulting in pain amplification and distortions. Traumatic injuries of the neural system such as spinal cord in...

Descripción completa

Detalles Bibliográficos
Autores principales: Gwak, Young S., Hulsebosch, Claire E., Leem, Joong Woo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5603132/
https://www.ncbi.nlm.nih.gov/pubmed/28951789
http://dx.doi.org/10.1155/2017/2480689
_version_ 1783264682723770368
author Gwak, Young S.
Hulsebosch, Claire E.
Leem, Joong Woo
author_facet Gwak, Young S.
Hulsebosch, Claire E.
Leem, Joong Woo
author_sort Gwak, Young S.
collection PubMed
description The hyperactive state of sensory neurons in the spinal cord enhances pain transmission. Spinal glial cells have also been implicated in enhanced excitability of spinal dorsal horn neurons, resulting in pain amplification and distortions. Traumatic injuries of the neural system such as spinal cord injury (SCI) induce neuronal hyperactivity and glial activation, causing maladaptive synaptic plasticity in the spinal cord. Recent studies demonstrate that SCI causes persistent glial activation with concomitant neuronal hyperactivity, thus providing the substrate for central neuropathic pain. Hyperactive sensory neurons and activated glial cells increase intracellular and extracellular glutamate, neuropeptides, adenosine triphosphates, proinflammatory cytokines, and reactive oxygen species concentrations, all of which enhance pain transmission. In addition, hyperactive sensory neurons and glial cells overexpress receptors and ion channels that maintain this enhanced pain transmission. Therefore, post-SCI neuronal-glial interactions create maladaptive synaptic circuits and activate intracellular signaling events that permanently contribute to enhanced neuropathic pain. In this review, we describe how hyperactivity of sensory neurons contributes to the maintenance of chronic neuropathic pain via neuronal-glial interactions following SCI.
format Online
Article
Text
id pubmed-5603132
institution National Center for Biotechnology Information
language English
publishDate 2017
publisher Hindawi
record_format MEDLINE/PubMed
spelling pubmed-56031322017-09-26 Neuronal-Glial Interactions Maintain Chronic Neuropathic Pain after Spinal Cord Injury Gwak, Young S. Hulsebosch, Claire E. Leem, Joong Woo Neural Plast Review Article The hyperactive state of sensory neurons in the spinal cord enhances pain transmission. Spinal glial cells have also been implicated in enhanced excitability of spinal dorsal horn neurons, resulting in pain amplification and distortions. Traumatic injuries of the neural system such as spinal cord injury (SCI) induce neuronal hyperactivity and glial activation, causing maladaptive synaptic plasticity in the spinal cord. Recent studies demonstrate that SCI causes persistent glial activation with concomitant neuronal hyperactivity, thus providing the substrate for central neuropathic pain. Hyperactive sensory neurons and activated glial cells increase intracellular and extracellular glutamate, neuropeptides, adenosine triphosphates, proinflammatory cytokines, and reactive oxygen species concentrations, all of which enhance pain transmission. In addition, hyperactive sensory neurons and glial cells overexpress receptors and ion channels that maintain this enhanced pain transmission. Therefore, post-SCI neuronal-glial interactions create maladaptive synaptic circuits and activate intracellular signaling events that permanently contribute to enhanced neuropathic pain. In this review, we describe how hyperactivity of sensory neurons contributes to the maintenance of chronic neuropathic pain via neuronal-glial interactions following SCI. Hindawi 2017 2017-08-29 /pmc/articles/PMC5603132/ /pubmed/28951789 http://dx.doi.org/10.1155/2017/2480689 Text en Copyright © 2017 Young S. Gwak et al. http://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
Gwak, Young S.
Hulsebosch, Claire E.
Leem, Joong Woo
Neuronal-Glial Interactions Maintain Chronic Neuropathic Pain after Spinal Cord Injury
title Neuronal-Glial Interactions Maintain Chronic Neuropathic Pain after Spinal Cord Injury
title_full Neuronal-Glial Interactions Maintain Chronic Neuropathic Pain after Spinal Cord Injury
title_fullStr Neuronal-Glial Interactions Maintain Chronic Neuropathic Pain after Spinal Cord Injury
title_full_unstemmed Neuronal-Glial Interactions Maintain Chronic Neuropathic Pain after Spinal Cord Injury
title_short Neuronal-Glial Interactions Maintain Chronic Neuropathic Pain after Spinal Cord Injury
title_sort neuronal-glial interactions maintain chronic neuropathic pain after spinal cord injury
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5603132/
https://www.ncbi.nlm.nih.gov/pubmed/28951789
http://dx.doi.org/10.1155/2017/2480689
work_keys_str_mv AT gwakyoungs neuronalglialinteractionsmaintainchronicneuropathicpainafterspinalcordinjury
AT hulseboschclairee neuronalglialinteractionsmaintainchronicneuropathicpainafterspinalcordinjury
AT leemjoongwoo neuronalglialinteractionsmaintainchronicneuropathicpainafterspinalcordinjury