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Molecular Links between Sensory Nerves, Inflammation, and Pain 3.0
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Molecular Links between Sensory Nerves, Inflammation, and Pain 3.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 February 2025 | Viewed by 8845

Special Issue Editors

Prof. Dr. Zsuzsanna Helyes

E-Mail Website
Guest Editor
Department of Pharmacology and Pharmacotherapy, Medical School & Szentagothai Research Centre, University of Pecs, H-7624 Pécs, Hungary
Interests: neuropharmacology; sensory nervous system; pain; inflammation; sensory-vascular-immune interactions; neuropathy; migraine; arthritis; TRP channels; neuroinflammation
Special Issues, Collections and Topics in MDPI journals
Dr. Szőke Éva

E-Mail Website
Guest Editor
Department of Pharmacology and Pharmacotherapy, Medical School, University of Pécs, H-7624 Pécs, Hungary
Interests: neuropharmacology; capsaicin; TRP channels; neuroinflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Capsaicin-sensitive peptidergic sensory nerves do not only transfer sensation and pain into the central nervous system (afferent function), but they also exert important efferent functions. They play complex regulatory roles in a broad range of inflammatory and pain conditions, such as arthritis/osteoarthritis, gastrointestinal diseases (irritable and inflammatory bowel diseases), neuropathic pain, and migraine. Several pro- and anti-inflammatory neuropeptides and other mediators (tachykinins, calcitonin gene-related peptide, pituitary adenylate cyclase-activating polypeptide, somatostatin, and purines) are released in response to their activation. Their balance and functions on immune cells and vessels determine the overall role of these nerves in different pathophysiological conditions related to unmet medical need diseases. Furthermore, inflammatory cell-derived mediators act back on these nerves to induce activation or inhibition. Exploring the molecular mechanisms of the complex sensory–immune–vascular interactions and identifying key targets can open promising novel anti-inflammatory and analgesic dug developmental perspectives.

Prof. Dr. Zsuzsanna Helyes
Dr. Szőke Éva
Guest Editors

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Keywords

  • sensory neuropeptides
  • inflammation
  • neurogenic inflammation
  • pain
  • arthritis
  • colitis
  • neuropathy
  • migraine
  • novel drug targets
  • TRP channels
  • neuroinflammation

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Related Special Issues

Published Papers (5 papers)

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Research

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18 pages, 1138 KiB  
Article
Dexmedetomidine as a Short-Use Analgesia for the Immature Nervous System
by Anatoliy Logashkin, Valentina Silaeva, Arsen Mamleev, Viktoria Shumkova, Violetta Sitdikova, Yaroslavna Popova, Dmitrii Suchkov and Marat Minlebaev
Int. J. Mol. Sci. 2024, 25(12), 6385; https://doi.org/10.3390/ijms25126385 - 9 Jun 2024
Cited by 1 | Viewed by 1238
Abstract
Pain management in neonates continues to be a challenge. Diverse therapies are available that cause loss of pain sensitivity. However, because of side effects, the search for better options remains open. Dexmedetomidine is a promising drug; it has shown high efficacy with a [...] Read more.
Pain management in neonates continues to be a challenge. Diverse therapies are available that cause loss of pain sensitivity. However, because of side effects, the search for better options remains open. Dexmedetomidine is a promising drug; it has shown high efficacy with a good safety profile in sedation and analgesia in the immature nervous system. Though dexmedetomidine is already in use for pain control in neonates (including premature neonates) and infants as an adjunct to other anesthetics, the question remains whether it affects the neuronal activity patterning that is critical for development of the immature nervous system. In this study, using the neonatal rat as a model, the pharmacodynamic effects of dexmedetomidine on the nervous and cardiorespiratory systems were studied. Our results showed that dexmedetomidine has pronounced analgesic effects in the neonatal rat pups, and also weakly modified both the immature network patterns of cortical and hippocampal activity and the physiology of sleep cycles. Though the respiration and heart rates were slightly reduced after dexmedetomidine administration, it might be considered as the preferential independent short-term therapy for pain management in the immature and developing brain. Full article
(This article belongs to the Special Issue Molecular Links between Sensory Nerves, Inflammation, and Pain 3.0)
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13 pages, 1768 KiB  
Article
Anti-Nociceptive Effects of Sphingomyelinase and Methyl-Beta-Cyclodextrin in the Icilin-Induced Mouse Pain Model
by Ádám Horváth, Anita Steib, Andrea Nehr-Majoros, Boglárka Kántás, Ágnes Király, Márk Racskó, Balázs István Tóth, Eszter Szánti-Pintér, Eva Kudová, Rita Skoda-Földes, Zsuzsanna Helyes and Éva Szőke
Int. J. Mol. Sci. 2024, 25(9), 4637; https://doi.org/10.3390/ijms25094637 - 24 Apr 2024
Viewed by 1185
Abstract
The thermo- and pain-sensitive Transient Receptor Potential Melastatin 3 and 8 (TRPM3 and TRPM8) ion channels are functionally associated in the lipid rafts of the plasma membrane. We have already described that cholesterol and sphingomyelin depletion, or inhibition of sphingolipid biosynthesis decreased the [...] Read more.
The thermo- and pain-sensitive Transient Receptor Potential Melastatin 3 and 8 (TRPM3 and TRPM8) ion channels are functionally associated in the lipid rafts of the plasma membrane. We have already described that cholesterol and sphingomyelin depletion, or inhibition of sphingolipid biosynthesis decreased the TRPM8 but not the TRPM3 channel opening on cultured sensory neurons. We aimed to test the effects of lipid raft disruptors on channel activation on TRPM3- and TRPM8-expressing HEK293T cells in vitro, as well as their potential analgesic actions in TRPM3 and TRPM8 channel activation involving acute pain models in mice. CHO cell viability was examined after lipid raft disruptor treatments and their effects on channel activation on channel expressing HEK293T cells by measurement of cytoplasmic Ca2+ concentration were monitored. The effects of treatments were investigated in Pregnenolone-Sulphate-CIM-0216-evoked and icilin-induced acute nocifensive pain models in mice. Cholesterol depletion decreased CHO cell viability. Sphingomyelinase and methyl-beta-cyclodextrin reduced the duration of icilin-evoked nocifensive behavior, while lipid raft disruptors did not inhibit the activity of recombinant TRPM3 and TRPM8. We conclude that depletion of sphingomyelin or cholesterol from rafts can modulate the function of native TRPM8 receptors. Furthermore, sphingolipid cleavage provided superiority over cholesterol depletion, and this method can open novel possibilities in the management of different pain conditions. Full article
(This article belongs to the Special Issue Molecular Links between Sensory Nerves, Inflammation, and Pain 3.0)
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Review

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25 pages, 2501 KiB  
Review
Update on Biomarkers of Chronic Inflammatory Processes Underlying Diabetic Neuropathy
by Adina Stoian, Carmen Muntean, Dragoș-Florin Babă, Andrei Manea, Lóránd Dénes, Zsuzsánna Simon-Szabó, Irina Bianca Kosovski, Enikő Nemes-Nagy, Florina Ioana Gliga and Mircea Stoian
Int. J. Mol. Sci. 2024, 25(19), 10395; https://doi.org/10.3390/ijms251910395 - 27 Sep 2024
Cited by 1 | Viewed by 2186
Abstract
There is an increasing prevalence of diabetes mellitus (DM), particularly type 2 DM (T2DM), and its associated complications. T2DM is linked to insulin resistance, chronic inflammation, and oxidative stress, which can lead to both macrovascular and microvascular complications, including peripheral diabetic neuropathy (PDN). [...] Read more.
There is an increasing prevalence of diabetes mellitus (DM), particularly type 2 DM (T2DM), and its associated complications. T2DM is linked to insulin resistance, chronic inflammation, and oxidative stress, which can lead to both macrovascular and microvascular complications, including peripheral diabetic neuropathy (PDN). Inflammatory processes play a key role in the development and progression of T2DM and its complications, with specific markers like C-reactive protein (CRP), interleukins (ILs), and tumor necrosis factor (TNF)-α being associated with increased risk. Other key inflammatory markers such as nuclear factor kappa B (NF-κB) are activated under hyperglycemic and oxidative stress conditions and contribute to the aggravation of PDN by regulating inflammatory gene expression and enhancing endothelial dysfunction. Other important roles in the inflammatory processes are played by Toll-like receptors (TLRs), caveolin 1 (CAV1), and monocyte chemoattractant protein 1 (MCP1). There is a relationship between vitamin D deficiency and PDN, highlighting the critical role of vitamin D in regulating inflammation and immune responses. The involvement of macrophages in PDN is also suspected, emphasizing their role in chronic inflammation and nerve damage in diabetic patients. Vitamin D supplementation has been found to reduce neuropathy severity, decrease inflammatory markers, and improve glycemic control. These findings suggest that addressing vitamin D deficiency could offer therapeutic benefits for PDN. These molecular pathways are critical in understanding the pathogenesis of DM complications and may offer potential biomarkers or therapeutic targets including anti-inflammatory treatments, vitamin D supplementation, macrophage phenotype modulation, and lifestyle modifications, aimed at reducing inflammation and preventing PDN. Ongoing and more extensive clinical trials with the aim of investigating anti-inflammatory agents, TNF-α inhibitors, and antioxidants are needed to advance deeper into the understanding and treatment of painful diabetic neuropathy. Full article
(This article belongs to the Special Issue Molecular Links between Sensory Nerves, Inflammation, and Pain 3.0)
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25 pages, 383 KiB  
Review
Exploring Localized Provoked Vulvodynia: Insights from Animal Model Research
by Yara Nakhleh-Francis, Yaseen Awad-Igbaria, Reem Sakas, Sarina Bang, Saher Abu-Ata, Eilam Palzur, Lior Lowenstein and Jacob Bornstein
Int. J. Mol. Sci. 2024, 25(8), 4261; https://doi.org/10.3390/ijms25084261 - 11 Apr 2024
Viewed by 2219
Abstract
Provoked vulvodynia represents a challenging chronic pain condition, characterized by its multifactorial origins. The inherent complexities of human-based studies have necessitated the use of animal models to enrich our understanding of vulvodynia’s pathophysiology. This review aims to provide an exhaustive examination of the [...] Read more.
Provoked vulvodynia represents a challenging chronic pain condition, characterized by its multifactorial origins. The inherent complexities of human-based studies have necessitated the use of animal models to enrich our understanding of vulvodynia’s pathophysiology. This review aims to provide an exhaustive examination of the various animal models employed in this research domain. A comprehensive search was conducted on PubMed, utilizing keywords such as “vulvodynia”, “chronic vulvar pain”, “vulvodynia induction”, and “animal models of vulvodynia” to identify pertinent studies. The search yielded three primary animal models for vulvodynia: inflammation-induced, allergy-induced, and hormone-induced. Additionally, six agents capable of triggering the condition through diverse pathways were identified, including factors contributing to hyperinnervation, mast cell proliferation, involvement of other immune cells, inflammatory cytokines, and neurotransmitters. This review systematically outlines the various animal models developed to study the pathogenesis of provoked vulvodynia. Understanding these models is crucial for the exploration of preventative measures, the development of novel treatments, and the overall advancement of research within the field. Full article
(This article belongs to the Special Issue Molecular Links between Sensory Nerves, Inflammation, and Pain 3.0)

Other

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9 pages, 3755 KiB  
Brief Report
Activation of Pedunculopontine Tegmental Nucleus Alleviates the Pain Induced by the Lesion of Midbrain Dopaminergic Neurons
by Shiqiang Zhang, Jingjing Zhang, Yihao Yang, Weidong Zang and Jing Cao
Int. J. Mol. Sci. 2024, 25(11), 5636; https://doi.org/10.3390/ijms25115636 - 22 May 2024
Cited by 1 | Viewed by 1284
Abstract
The loss of midbrain dopaminergic (DA) neurons is the fundamental pathological feature of Parkinson’s disease (PD). PD causes chronic pain in two-thirds of patients. Recent studies showed that the activation of the pedunculopontine tegmental nucleus (PPTg) can effectively relieve inflammatory pain and neuropathic [...] Read more.
The loss of midbrain dopaminergic (DA) neurons is the fundamental pathological feature of Parkinson’s disease (PD). PD causes chronic pain in two-thirds of patients. Recent studies showed that the activation of the pedunculopontine tegmental nucleus (PPTg) can effectively relieve inflammatory pain and neuropathic pain. The PPTg is located in the pontomesencephalic tegmentum, a target of deep brain stimulation (DBS) treatment in PD, and is involved in motor control and sensory integration. To test whether the lesion of midbrain DA neurons induced pain hypersensitivity, and whether the chemogenetic activation of the PPTg could modulate the pain, the AAV-hM3Dq receptor was transfected and expressed into the PPTg neurons of 6-hydroxydopamine-lesioned mice. In this study, von Frey, open field, and adhesive tape removal tests were used to assess animals’ pain sensitivity, locomotor activity, and sensorimotor function and somatosensory perception, respectively. Here, we found that the lesion of midbrain DA neurons induced a minor deficit in voluntary movement but did not affect sensorimotor function and somatosensory perception in the tape removal test. The results showed that lesion led to pain hypersensitivity, which could be alleviated both by levodopa and by the chemogenetic activation of the PPTg. Activating the PPTg may be a potential therapeutic strategy to relieve pain phenotypes in PD. Full article
(This article belongs to the Special Issue Molecular Links between Sensory Nerves, Inflammation, and Pain 3.0)
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