Editorial Maladaptive Plasticity and Neuropathic...
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Editorial Maladaptive Plasticity and Neuropathic Pain Xiang-Yao Li, 1 You Wan, 2 Shao-Jun Tang, 3 Yun Guan, 4 Feng Wei, 5 and Daqing Ma 6 1 Institute of Neuroscience and Collaborative Innovation Center for Brain Science, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310058, China 2 Department of Neurobiology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China 3 Department of Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, TX 77555, USA 4 Department of Anesthesiology and Critical Care Medicine, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA 5 Department of Neural and Pain Sciences, Dental School, Program in Neuroscience, University of Maryland, 650 W. Baltimore Street, Baltimore, MD 21201, USA 6 Anaesthetics, Pain Medicine and Intensive Care, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, Chelsea & Westminster Hospital, London SW10 9NH, UK Correspondence should be addressed to Xiang-Yao Li; [email protected] Received 27 October 2015; Accepted 28 October 2015 Copyright © 2016 Xiang-Yao Li et al. is 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. e neuropathic pain is caused by the injury or damage on the sensory nervous system; its pathological manifestations include allodynia, hyperalgesia, and spontaneous pain. About 4–8% of people in our society are suffering from this disease. e maladaptive plasticity refers to the plasticity in the nervous system that leads to a disruption of the function and may be considered as a disease state [1]. Emerging evidences from both human patients and animal models showed that maladaptive plastic changes happened along the sensory pathways, from the peripheral to central nervous system, which may contribute to the generation, development, and maintenance of neuropathic pain. e current special issue focused on the molecular mechanism underlying maladap- tive plasticity along sensory pathways; different laboratories around the world investigated the maladaptive change in different signaling pathways at different levels; the contribu- tions in this area will highlight the pain managements in the future. e transient receptor potential cation channel subfamily V member 1 (TRPV1) is the first identified member of TRPV proteins. TRPV1 can be activated by high temperature or specific chemical stimuli. e activation of TRPV1 in the terminal of nociceptive primary afferents conveys noxious information to the spinal cord and superspinal regions. Recent studies also identified critical roles of TRPV1 in the central regions of pain pathway in pain regulation. In the current issue, T. Jian et al. report that TRPV1 in dorsal root ganglia (DRG) modulates histamine H4 receptor-mediated itch. is finding will extend our understanding of the mechanisms of histamine-induced itch and the interaction of the itch and pain. S.-I. Choi et al. review recent studies on TRPV1-regulated pain, especially pathological pain, and suggest that TRPV1 contributes to pain maintenance. e new data may have revealed novel insights into the roles of spinal cord TRPV1 in regulating spinal plasticity, which may identify a new target for modulating pathological pain. Low back pain affects a large number of patients. Defor- mation of DRGs and their nerve roots is implicated in the pathogenesis. W.-J. Han et al. evaluate the analgesic effects of a novel synthesized nitronyl (NIT) nitroxide radicals on radicular low back pain in a rat model generated by chronic DRG compression. e authors report a significant analgesic effect of this agent, probably due to its antioxidation and anti- inflammation effects. Y-.B. Xie et al. describe a new rat animal model of human low back pain, by chronic compression of multiple DRGs on one side of lumber. is rat model develops spontaneous pain, cold allodynia, and hyperalgesia. Activating transcription factor 3 (ATF3) and CGRP are upregulated in bilateral DRG neurons and may contribute to the expression of DRG compression-induced pain. Matrix metalloproteinases (MMPs) play important roles in nociception and allodynia. Q. Wang et al. report a crit- ical role of Extracellular Matrix Metalloproteinase Inducer (EMMPRIN)/OX47, a key regulator of MMP activities, in Hindawi Publishing Corporation Neural Plasticity Volume 2016, Article ID 4842159, 2 pages http://dx.doi.org/10.1155/2016/4842159
Transcript of Editorial Maladaptive Plasticity and Neuropathic...
EditorialMaladaptive Plasticity and Neuropathic Pain
Xiang-Yao Li,1 You Wan,2 Shao-Jun Tang,3 Yun Guan,4 Feng Wei,5 and Daqing Ma6
1 Institute of Neuroscience and Collaborative Innovation Center for Brain Science, School of Medicine, Zhejiang University,Hangzhou, Zhejiang 310058, China2Department of Neurobiology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China3Department of Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, TX 77555, USA4Department of Anesthesiology and Critical Care Medicine, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA5Department of Neural and Pain Sciences, Dental School, Program in Neuroscience, University of Maryland,650 W. Baltimore Street, Baltimore, MD 21201, USA6Anaesthetics, Pain Medicine and Intensive Care, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London,Chelsea &Westminster Hospital, London SW10 9NH, UK
Correspondence should be addressed to Xiang-Yao Li; [email protected]
Received 27 October 2015; Accepted 28 October 2015
Copyright © 2016 Xiang-Yao Li 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 neuropathic pain is caused by the injury or damage onthe sensory nervous system; its pathological manifestationsinclude allodynia, hyperalgesia, and spontaneous pain. About4–8% of people in our society are suffering from this disease.The maladaptive plasticity refers to the plasticity in thenervous system that leads to a disruption of the function andmay be considered as a disease state [1]. Emerging evidencesfrom both human patients and animal models showed thatmaladaptive plastic changes happened along the sensorypathways, from the peripheral to central nervous system,which may contribute to the generation, development, andmaintenance of neuropathic pain. The current special issuefocused on the molecular mechanism underlying maladap-tive plasticity along sensory pathways; different laboratoriesaround the world investigated the maladaptive change indifferent signaling pathways at different levels; the contribu-tions in this area will highlight the pain managements in thefuture.
The transient receptor potential cation channel subfamilyV member 1 (TRPV1) is the first identified member of TRPVproteins. TRPV1 can be activated by high temperature orspecific chemical stimuli. The activation of TRPV1 in theterminal of nociceptive primary afferents conveys noxiousinformation to the spinal cord and superspinal regions.Recent studies also identified critical roles of TRPV1 in thecentral regions of pain pathway in pain regulation. In thecurrent issue, T. Jian et al. report that TRPV1 in dorsal root
ganglia (DRG) modulates histamine H4 receptor-mediateditch. This finding will extend our understanding of themechanisms of histamine-induced itch and the interactionof the itch and pain. S.-I. Choi et al. review recent studieson TRPV1-regulated pain, especially pathological pain, andsuggest that TRPV1 contributes to pain maintenance. Thenew data may have revealed novel insights into the roles ofspinal cord TRPV1 in regulating spinal plasticity, which mayidentify a new target for modulating pathological pain.
Low back pain affects a large number of patients. Defor-mation of DRGs and their nerve roots is implicated in thepathogenesis. W.-J. Han et al. evaluate the analgesic effectsof a novel synthesized nitronyl (NIT) nitroxide radicals onradicular low back pain in a rat model generated by chronicDRG compression. The authors report a significant analgesiceffect of this agent, probably due to its antioxidation and anti-inflammation effects. Y-.B. Xie et al. describe a new rat animalmodel of human low back pain, by chronic compressionof multiple DRGs on one side of lumber. This rat modeldevelops spontaneous pain, cold allodynia, and hyperalgesia.Activating transcription factor 3 (ATF3) and CGRP areupregulated in bilateral DRG neurons and may contribute tothe expression of DRG compression-induced pain.
Matrix metalloproteinases (MMPs) play important rolesin nociception and allodynia. Q. Wang et al. report a crit-ical role of Extracellular Matrix Metalloproteinase Inducer(EMMPRIN)/OX47, a key regulator of MMP activities, in
Hindawi Publishing CorporationNeural PlasticityVolume 2016, Article ID 4842159, 2 pageshttp://dx.doi.org/10.1155/2016/4842159
2 Neural Plasticity
neuropathic pain development. Their studies show that SNLleads to OX47 upregulation in ipsilateral DRG and thatdownregulation of OX47 attenuates SNL-induced mechani-cal allodynia.
Gate-control theory of pain proposed by Melzack andWall (1965) explains the regulation of noxious informationtransmission in the spinal substantia gelatinosa. F. J. R.Pelaez and S. Taniguchi have revisited this theory from theperspective of NMDA receptor-mediated synaptic plasticityand intrinsic plasticity, and the Melzack and Wall circuitwas slightly modified by using strictly excitatory nociceptiveafferences and was further tested at different pain conditions.
Spinal microglia play critical roles in the developmentsof chronic pain. A. Jurga et al. report the contribution ofTLR2 and TLR4 to neuropathic pain in a chronic constric-tion injury (CCI) model. They describe a time-dependentupregulation of TLR2, TLR4, MyD88, and TRIF mRNA andprotein. In addition, blockade of TLR2 and TLR4 impairsthe expression of pain behaviors and opioid analgesia. Thesefindings support TLR2 and TLR4 as putative targets fordeveloping therapeutic approaches.
J. Wang et al. report the involvements of mammalian tar-get of rapamycin (mTOR) in the RVM, a key relay region forthe descending pathway, in regulation of neuropathic pain.They show that phosphorylated mTOR protein increasesmainly in RVM serotonergic spinally projecting neurons inthe spared nerve injury (SNI) model. Infusion of rapamycindecreases both excitatory synaptic transmission and intrinsicexcitability of serotonergic neurons, which may underlie theanalgesic effects. These findings suggest a novel mechanismby which mTOR inhibitor causes analgesia.
The anterior cingulate cortex (ACC) is a heterogeneousbrain region and is involved in regulation of pain, emotion,and sex attraction. Z.-X. Zuo et al. report that nerve ligationleads to AChE upregulation in the ACC.They have tested theanalgesic effects of huperzine A, an alkaloid isolated from aChinese club-moss, on evoked pain and spontaneous pain,and reported a significant analgesic effect on evoked pain butnot spontaneous pain, indicating a specific role of AChE inregulation of evoked pain.
We are pleased to introduce this special issue that focuseson themaladaptive plasticity in the pain pathway, in bothPNSand CNS. It is becoming clear that pain-related maladaptivechanges can occur at a cellular level such as alteration ofsynaptic transmission and at a molecular level such as thedysregulation of various signaling pathways. The studiescollected in this issue will help elucidate the pathogenicmechanism of neuropathic pain and facilitate the develop-ment of novel strategies for the pain treatments.
Acknowledgments
We would like to thank all authors and reviewers for theiressential contribution to this special issue.
Xiang-Yao LiYou Wan
Shao-Jun TangYun GuanFeng Wei
Daqing Ma
References
[1] C. J. Woolf, “Recent advances in the pathophysiology of acutepain,” British Journal of Anaesthesia, vol. 63, no. 2, pp. 139–146,1989.
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