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Cellular Mechanisms in Neuropathic Pain
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Cellular Mechanisms in Neuropathic Pain

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

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 12959

Special Issue Editors

Dr. Young-seob Gwak

E-Mail Website
Guest Editor
Department of Anesthesioogy and Perioperative Care, Irvine, CA, USA
Interests: chronic pain; spinal cord injury; peripheral nerve injury; synaptic plasticity; synaptic reorganization
Prof. Dr. Joong Woo Leem

E-Mail Website
Guest Editor
Department of Physiology, Yonsei University College of Medicine, Seoul 03722, Korea
Interests: neuropathic pain; inflammatory pain; pain modulation; Nociceptors; Spinal cord plasticity; Analgesia

Special Issue Information

Dear Colleagues,

Chronic pain limits the personal activity and negatively affects the quality of life. Increasing evidence in preclinical research suggests that the imbalance between excitatory and inhibitory tone, followed by the development and maintenance of sensory neuronal hyperexcitability, plays a key role in chronic neuropathic pain. In the nervous system, the tripartite structures composed of presynaptic, postsynaptic and surrounding glial cells maintain the homeostatic regulation of sensory synaptic transmission. However, the pathophysiological condition causes the maladaptation of those synaptic structures that result in the development of hyperexcitable status in sensory neurons and cause increases in spontaneous and evoked firing rates via decreased thresholds for neuronal activation and long-lasting firing patterns in the spinal cord, brain stem, and brain. That enhanced sensory neuronal firing activity directly converts into allodynic and hyperalgesic behaviors. Therefore, providing clear insight into altered mechanisms of cellular processing will provide an appropriate treatment strategy for neuropathic pain. This Special Issue welcomes original research or systematic review articles providing basic insights into the cellular mechanism of neuropathic pain.

Dr. Young-seob Gwak
Prof. Dr. Joong Woo Leem
Guest Editors

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Keywords

  • spinal cord injury pain
  • peripheral nerve injury pain
  • orofacial pain
  • diabetic neuropathic pain
  • hyperexcitability
  • synaptic plasticity
  • analgesia
  • pain modulation

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Published Papers (4 papers)

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Research

17 pages, 1947 KiB  
Article
Time-Dependent Changes in Protein Composition of Medial Prefrontal Cortex in Rats with Neuropathic Pain
by Hana Ujcikova, Dagoberto Robles, Xu Yue, Petr Svoboda, Yeon Sun Lee and Edita Navratilova
Int. J. Mol. Sci. 2022, 23(2), 955; https://doi.org/10.3390/ijms23020955 - 16 Jan 2022
Cited by 7 | Viewed by 2802
Abstract
Chronic pain is associated with time-dependent structural and functional reorganization of the prefrontal cortex that may reflect adaptive pain compensatory and/or maladaptive pain-promoting mechanisms. However, the molecular underpinnings of these changes and whether there are time-dependent relationships to pain progression are not well [...] Read more.
Chronic pain is associated with time-dependent structural and functional reorganization of the prefrontal cortex that may reflect adaptive pain compensatory and/or maladaptive pain-promoting mechanisms. However, the molecular underpinnings of these changes and whether there are time-dependent relationships to pain progression are not well characterized. In this study, we analyzed protein composition in the medial prefrontal cortex (mPFC) of rats at two timepoints after spinal nerve ligation (SNL) using two-dimensional gel electrophoresis (2D-ELFO) and liquid chromatography with tandem mass spectrometry (LC–MS/MS). SNL, but not sham-operated, rats developed persistent tactile allodynia and thermal hyperalgesia, confirming the presence of experimental neuropathic pain. Two weeks after SNL (early timepoint), we identified 11 proteins involved in signal transduction, protein transport, cell homeostasis, metabolism, and apoptosis, as well as heat-shock proteins and chaperones that were upregulated by more than 1.5-fold compared to the sham-operated rats. Interestingly, there were only four significantly altered proteins identified at 8 weeks after SNL (late timepoint). These findings demonstrate extensive time-dependent modifications of protein expression in the rat mPFC under a chronic neuropathic pain state that might underlie the evolution of chronic pain characterized by early pain-compensatory and later aberrant mechanisms. Full article
(This article belongs to the Special Issue Cellular Mechanisms in Neuropathic Pain)
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14 pages, 2129 KiB  
Article
Magnesium and Morphine in the Treatment of Chronic Neuropathic Pain–A Biomedical Mechanism of Action
by Kamila Kulik, Barbara Żyżyńska-Granica, Agnieszka Kowalczyk, Przemysław Kurowski, Małgorzata Gajewska and Magdalena Bujalska-Zadrożny
Int. J. Mol. Sci. 2021, 22(24), 13599; https://doi.org/10.3390/ijms222413599 - 18 Dec 2021
Cited by 10 | Viewed by 3300
Abstract
The effectiveness of opioids in the treatment of neuropathic pain is limited. It was demonstrated that magnesium ions (Mg2+), physiological antagonists of N-methyl-D-aspartate receptor (NMDAR), increase opioid analgesia in chronic pain. Our study aimed to determine the molecular mechanism of this [...] Read more.
The effectiveness of opioids in the treatment of neuropathic pain is limited. It was demonstrated that magnesium ions (Mg2+), physiological antagonists of N-methyl-D-aspartate receptor (NMDAR), increase opioid analgesia in chronic pain. Our study aimed to determine the molecular mechanism of this action. Early data indicate the cross-regulation of µ opioid receptor (MOR) and NMDAR in pain control. Morphine acting on MOR stimulates protein kinase C (PKC), while induction of NMDAR recruits protein kinase A (PKA), leading to a disruption of the MOR-NMDAR complex and promoting functional changes in receptors. The mechanical Randall-Selitto test was used to assess the effect of chronic Mg2+ and morphine cotreatment on streptozotocin-induced hyperalgesia in Wistar rats. The level of phosphorylated NMDAR NR1 subunit (pNR1) and phosphorylated MOR (pMOR) in the periaqueductal gray matter was determined with the Western blot method. The activity of PKA and PKC was examined by standard enzyme immunoassays. The experiments showed a reduction in hyperalgesia after coadministration of morphine (5 mg/kg intraperitoneally) and Mg2+ (40 mg/kg intraperitoneally). Mg2+ administered alone significantly decreased the level of pNR1, pMOR, and activity of both tested kinases. The results suggest that blocking NMDAR signaling by Mg2+ restores the MOR-NMDAR complex and thus enables morphine analgesia in neuropathic rats. Full article
(This article belongs to the Special Issue Cellular Mechanisms in Neuropathic Pain)
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19 pages, 2852 KiB  
Article
The Clinical Application of Pulsed Radiofrequency Induces Inflammatory Pain via MAPKs Activation: A Novel Hint for Pulsed Radiofrequency Treatment
by Feng-Yen Lin, Kuo-Feng Huang, Jui-Chieh Chen, Meng-Fu Lai, Kuo-Hsing Ma and Chun-Chang Yeh
Int. J. Mol. Sci. 2021, 22(21), 11865; https://doi.org/10.3390/ijms222111865 - 1 Nov 2021
Cited by 9 | Viewed by 3454
Abstract
Pulsed radiofrequency (PRF) works by delivering short bursts of radiofrequency to a target nerve, thereby affecting nerve signal transduction to reduce pain. Although preliminary clinical investigations have shown that PRF treatment can be used safely as an alternative interventional treatment in patients with [...] Read more.
Pulsed radiofrequency (PRF) works by delivering short bursts of radiofrequency to a target nerve, thereby affecting nerve signal transduction to reduce pain. Although preliminary clinical investigations have shown that PRF treatment can be used safely as an alternative interventional treatment in patients with refractory pain conditions, unexpected damage to a normal nerve/ganglion is still one of the possible complications of using the PRF strategy. Noxious pain may also be triggered if PRF treatment accidentally damages an intact nerve. However, few studies in the literature have described the intracellular modifications that occur in neuronal cells after PRF stimulation. Therefore, in this study, we evaluated the effects of PRF on unimpaired nerve function and investigated the potential mechanisms of PRF-induced pain. Wistar rats were stimulated with 30–60 V of PRF for 6 min, and mechanical allodynia, cold hypersensitivity, cytokine and matrix metalloproteinase (MMP) production, and mitogen-activated protein kinase activity (p38 MAPK, ERK1/2, JNK/SAPK) were analyzed. The results indicated that PRF stimulation induced a significant algesic effect and nociceptive response. In addition, the protein array and Western blotting analyses showed that the clinical application of 60 V of PRF can induce the activation of MAPKs and the production of inflammatory cytokines and MMPs in the lumbar dorsal horn, which is necessary for nerve inflammation, and it can be suppressed by MAPK antagonist treatment. These results indicate that PRF stimulation may induce inflammation of the intact nerve, which in turn causes inflammatory pain. This conclusion can also serve as a reminder for PRF treatment of refractory pain. Full article
(This article belongs to the Special Issue Cellular Mechanisms in Neuropathic Pain)
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24 pages, 2759 KiB  
Article
Comparison of the Effects of Chemokine Receptors CXCR2 and CXCR3 Pharmacological Modulation in Neuropathic Pain Model—In Vivo and In Vitro Study
by Anna Piotrowska, Katarzyna Ciapała, Katarzyna Pawlik, Klaudia Kwiatkowski, Ewelina Rojewska and Joanna Mika
Int. J. Mol. Sci. 2021, 22(20), 11074; https://doi.org/10.3390/ijms222011074 - 14 Oct 2021
Cited by 16 | Viewed by 2733
Abstract
Recent findings have highlighted the roles of CXC chemokine family in the mechanisms of neuropathic pain. Our studies provide evidence that single/repeated intrathecal administration of CXCR2 (NVP-CXCR2-20) and CXCR3 ((±)-NBI-74330) antagonists explicitly attenuated mechanical/thermal hypersensitivity in rats after chronic constriction injury of the [...] Read more.
Recent findings have highlighted the roles of CXC chemokine family in the mechanisms of neuropathic pain. Our studies provide evidence that single/repeated intrathecal administration of CXCR2 (NVP-CXCR2-20) and CXCR3 ((±)-NBI-74330) antagonists explicitly attenuated mechanical/thermal hypersensitivity in rats after chronic constriction injury of the sciatic nerve. After repeated administration, both antagonists showed strong analgesic activity toward thermal hypersensitivity; however, (±)-NBI-74330 was more effective at reducing mechanical hypersensitivity. Interestingly, repeated intrathecal administration of both antagonists decreased the mRNA and/or protein levels of pronociceptive interleukins (i.e., IL-1beta, IL-6, IL-18) in the spinal cord, but only (±)-NBI-74330 decreased their levels in the dorsal root ganglia after nerve injury. Furthermore, only the CXCR3 antagonist influenced the spinal mRNA levels of antinociceptive factors (i.e., IL-1RA, IL-10). Additionally, antagonists effectively reduced the mRNA levels of pronociceptive chemokines; NVP-CXCR2-20 decreased the levels of CCL2, CCL6, CCL7, and CXCL4, while (±)-NBI-74330 reduced the levels of CCL3, CCL6, CXCL4, and CXCL9. Importantly, the results obtained from the primary microglial and astroglial cell cultures clearly suggest that both antagonists can directly affect the release of these ligands, mainly in microglia. Interestingly, NVP-CXCR2-20 induced analgesic effects after intraperitoneal administration. Our research revealed important roles for CXCR2 and CXCR3 in nociceptive transmission, especially in neuropathic pain. Full article
(This article belongs to the Special Issue Cellular Mechanisms in Neuropathic Pain)
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