Regional Hyperexcitability and Chronic Neuropathic Pain Following Spinal Cord Injury
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REVIEW PAPER
Regional Hyperexcitability and Chronic Neuropathic Pain Following Spinal Cord Injury Jonghoon Kang1 · Steve S. Cho2 · Hee Young Kim3 · Bong Hyo Lee4 · Hee Jung Cho5 · Young S. Gwak3 Received: 17 April 2019 / Accepted: 2 January 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Spinal cord injury (SCI) causes maladaptive changes to nociceptive synaptic circuits within the injured spinal cord. Changes also occur at remote regions including the brain stem, limbic system, cortex, and dorsal root ganglia. These maladaptive nociceptive synaptic circuits frequently cause neuronal hyperexcitability in the entire nervous system and enhance nociceptive transmission, resulting in chronic central neuropathic pain following SCI. The underlying mechanism of chronic neuropathic pain depends on the neuroanatomical structures and electrochemical communication between pre- and postsynaptic neuronal membranes, and propagation of synaptic transmission in the ascending pain pathways. In the nervous system, neurons are the only cell type that transmits nociceptive signals from peripheral receptors to supraspinal systems due to their neuroanatomical and electrophysiological properties. However, the entire range of nociceptive signaling is not mediated by any single neuron. Current literature describes regional studies of electrophysiological or neurochemical mechanisms for enhanced nociceptive transmission post-SCI, but few studies report the electrophysiological, neurochemical, and neuroanatomical changes across the entire nervous system following a regional SCI. We, along with others, have continuously described the enhanced nociceptive transmission in the spinal dorsal horn, brain stem, thalamus, and cortex in SCI-induced chronic central neuropathic pain condition, respectively. Thus, this review summarizes the current understanding of SCI-induced neuronal hyperexcitability and maladaptive nociceptive transmission in the entire nervous system that contributes to chronic central neuropathic pain. Keywords Spinal cord injury · Neuropathic pain · Hyperexcitability
Introduction Spinal cord injury (SCI) causes direct and indirect spinal damage that results in temporal and spatial changes to neurochemical and neuroanatomical features in the nervous system. Glutamate, GABA, serotonin, reactive oxygen species (ROS), and proinflammatory cytokines are the
predominant substrates in neurochemical shifts (Hains et al. 2002; Guptarak et al. 2013; Gwak et al. 2013; McAdoo and Wu 2008; Vaziri et al. 2004), whereas altered expressions of receptors/ion channels, sprouting/denervation of primary afferent fibers, and glial activations are predominant features in neuroanatomical shifts in rodent SCI models (Dunlop 2008; Hama and Sagen 2011; Mills et al. 2001). These
* Hee Jung Cho [email protected]
1
Department of Biology, Valdosta State University, Valdosta, GA 31698, USA
* Young S. Gwak [email protected]
2
Department of Ophthalmology, Boston Children’s Hospital, Harvard Medical School, Boston,
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