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...
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| Language: | English |
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Wiley
2017-01-01
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| Series: | Neural Plasticity |
| Online Access: | http://dx.doi.org/10.1155/2017/2480689 |
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| author | Young S. Gwak Claire E. Hulsebosch Joong Woo Leem |
| author_facet | Young S. Gwak Claire E. Hulsebosch Joong Woo Leem |
| author_sort | Young S. Gwak |
| collection | DOAJ |
| 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 | Article |
| id | doaj-art-c9e55eebf28a480aa4d0ad6ebd5a0239 |
| institution | OA Journals |
| issn | 2090-5904 1687-5443 |
| language | English |
| publishDate | 2017-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Neural Plasticity |
| spelling | doaj-art-c9e55eebf28a480aa4d0ad6ebd5a02392025-08-20T02:19:42ZengWileyNeural Plasticity2090-59041687-54432017-01-01201710.1155/2017/24806892480689Neuronal-Glial Interactions Maintain Chronic Neuropathic Pain after Spinal Cord InjuryYoung S. Gwak0Claire E. Hulsebosch1Joong Woo Leem2Department of Physiology, College of Korean Medicine, Daegu Haany University, Daegu, Republic of KoreaDepartment of Neurobiology and Anatomy, The University of Texas Health Science Center at Houston, Houston, TX 77030, USADepartment of Physiology, Yonsei University College of Medicine, Seoul, Republic of KoreaThe 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.http://dx.doi.org/10.1155/2017/2480689 |
| spellingShingle | Young S. Gwak Claire E. Hulsebosch Joong Woo Leem Neuronal-Glial Interactions Maintain Chronic Neuropathic Pain after Spinal Cord Injury Neural Plasticity |
| 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 |
| url | http://dx.doi.org/10.1155/2017/2480689 |
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