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Neural Plasticity
Volume 2017, Article ID 2480689, 14 pages
Review Article

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

1Department of Physiology, College of Korean Medicine, Daegu Haany University, Daegu, Republic of Korea
2Department of Neurobiology and Anatomy, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA
3Department of Physiology, Yonsei University College of Medicine, Seoul, Republic of Korea

Correspondence should be addressed to Claire E. Hulsebosch; ude.cmt.htu@hcsobesluH.erialC and Joong Woo Leem; ca.shuy@meelwj

Received 17 April 2017; Revised 26 June 2017; Accepted 5 July 2017; Published 29 August 2017

Academic Editor: Mauricio A. Retamal

Copyright © 2017 Young S. Gwak et al. 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.


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.