Molecular Mechanisms of Neuropathic Pain

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 703

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Guest Editor
Emer. Prof. of Nagasaki Univ. Laboratory for the Study of Pain Research Institute for Production Development 15 Shimogamo Morimoto-cho, Sakyo-ku, Kyoto 606-0805, Japan
Interests: prothymosin α; stroke; DAMPs/alarmins; chronic pain; fibromyalgia; opioid receptor
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Department of Pharmacology, Graduate School of Biomedical Sciences, Hiroshima University, Kasumi 1-2-3, Minami-ku, Hiroshima 734–8551, Japan
Interests: proinflammatory cytokines; neuroprharmacology; connexin43

Special Issue Information

Dear Colleagues,

With the ageing of the global population and the social instability caused by various epidemics, disasters and conflicts, the number of patients with chronic pain continues to increase. According to a recent proposal, nociplastic pain such as fibromyalgia is categorized as both a chronic and neuropathic pain. Some medicines that are able to treat chronic pain are now available, but they often have effects events during long-term treatments. Ideally, we should consider short-term and radical treatments that suppress the pain memory. For this purpose, it is necessary to clarify the mechanisms of prolonged pain and search for new mechanism-based drug targets. Over the past decade, pain research has focused on primary sensory nerves and spinal dorsal horn, and has yielded numerous findings. More recent studies have revealed that repeated pain stimuli also affect various brain regions and that changes in the structure and function of neural networks may contribute to prolonged pain. This Special Issue, therefore, focuses on the latest findings underlying the pain persistence associated with changes in the neural networks mediated by neurons, glial cells and immune cells in various brain regions, and with the brain–immune connection in the development of chronic pain.

Prof. Dr. Hiroshi Ueda
Prof. Dr. Norimitsu Morioka
Guest Editors

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Keywords

  • neuropathic pain
  • nociplastic pain
  • fibromyalgia
  • brain-immune connection
  • sexual dimorphism
  • glial cells
  • lysophosphatidic acid

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Published Papers (1 paper)

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Research

11 pages, 1116 KiB  
Communication
Effects of Tryptophan and Physical Exercise on the Modulation of Mechanical Hypersensitivity in a Fibromyalgia-like Model in Female Rats
by Rafael Marins Rezende, Roney Santos Coimbra, Markus Kohlhoff, Lukiya Silva Campos Favarato, Hércia Stampini Duarte Martino, Luciano Bernardes Leite, Leoncio Lopes Soares, Samuel Encarnação, Pedro Forte, António Miguel de Barros Monteiro, Maria do Carmo Gouveia Peluzio and Antônio José Natali
Cells 2024, 13(19), 1647; https://doi.org/10.3390/cells13191647 - 3 Oct 2024
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Abstract
Though the mechanisms are not fully understood, tryptophan (Trp) and physical exercise seem to regulate mechanical hypersensitivity in fibromyalgia. Here, we tested the impact of Trp supplementation and continuous low-intensity aerobic exercise on the modulation of mechanical hypersensitivity in a fibromyalgia-like model induced [...] Read more.
Though the mechanisms are not fully understood, tryptophan (Trp) and physical exercise seem to regulate mechanical hypersensitivity in fibromyalgia. Here, we tested the impact of Trp supplementation and continuous low-intensity aerobic exercise on the modulation of mechanical hypersensitivity in a fibromyalgia-like model induced by acid saline in female rats. Twelve-month-old female Wistar rats were randomly divided into groups: [control (n = 6); acid saline (n = 6); acid saline + exercise (n = 6); acid saline + Trp (n = 6); and acid saline + exercise + Trp (n = 6)]. Hypersensitivity was caused using two intramuscular jabs of acid saline (20 μL; pH 4.0; right gastrocnemius), 3 days apart. The tryptophan-supplemented diet contained 7.6 g/hg of Trp. The three-week exercise consisted of progressive (30–45 min) treadmill running at 50 to 60% intensity, five times (Monday to Friday) per week. We found that acid saline induced contralateral mechanical hypersensitivity without changing the levels of Trp, serotonin (5-HT), and kynurenine (KYN) in the brain. Hypersensitivity was reduced by exercise (~150%), Trp (~67%), and its combination (~160%). The Trp supplementation increased the levels of Trp and KYN in the brain, and the activity of indoleamine 2,3-dioxygenase (IDO), and decreased the ratio 5-HT:KYN. Exercise did not impact the assessed metabolites. Combining the treatments reduced neither hypersensitivity nor the levels of serotonin and Trp in the brain. In conclusion, mechanical hypersensitivity induced by acid saline in a fibromyalgia-like model in female rats is modulated by Trp supplementation, which increases IDO activity and leads to improved Trp metabolism via the KYN pathway. In contrast, physical exercise does not affect mechanical hypersensitivity through brain Trp metabolism via either the KYN or serotonin pathways. Because this is a short study, generalizing its findings warrants caution. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Neuropathic Pain)
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