ArticleNeuroscience bulletin2018
Involvement of NF-κB and the CX3CR1 Signaling Network in Mechanical Allodynia Induced by Tetanic Sciatic Stimulation.
Article in Neuroscience bulletin, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Scutellarin Alleviates Neuronal Apoptosis After Ischemia and Hypoxia via the HIF-1α-CX3CR1 Axis.CNS neuroscience & therapeutics · 2026Article
- Unraveling the immune system's role in peripheral nerve regeneration: a pathway to enhanced healing.Frontiers in immunology · 2025Review
- Neuroplasticity in the transition from acute to chronic pain.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Review
- HDAC inhibitors as a potential therapy for chemotherapy-induced neuropathic pain.Inflammopharmacology · 2024Review
- HIV-Associated Neurocognitive Disorder: A Look into Cellular and Molecular Pathology.International journal of molecular sciences · 2024Review
- Glabridin Therapy Reduces Chronic Allodynia, Spinal Microgliosis, and Dendritic Spine Generation by Inhibiting Fractalkine-CX3CR1 Signaling in a Mouse Model of Tibial Fractures.Brain sciences · 2023Article
- Fractalkine/CX3CR1-Dependent Modulation of Synaptic and Network Plasticity in Health and Disease.Neural plasticity · 2023Review
- Targeting Vascular endothelial growth factor A with soluble vascular endothelial growth factor receptor 1 ameliorates nerve injury-induced neuropathic pain.Molecular pain · 2022Article
- Mechanistic Insight into the Effects of Curcumin on Neuroinflammation-Driven Chronic Pain.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Peripheral Nervous System Involvement in Non-Primary Pediatric Cancer: From Neurotoxicity to Possible Etiologies.Journal of clinical medicine · 2021Review
- TLR8 in the Trigeminal Ganglion Contributes to the Maintenance of Trigeminal Neuropathic Pain in Mice.Neuroscience bulletin · 2021Article
- PDTC ameliorates neuropathic pain by inhibiting microglial activation <em>via</em> blockage of the TNFα-CX3CR1 pathway.European journal of histochemistry : EJH · 2021Article
- PPAR γ Prevents Neuropathic Pain by Down-Regulating CX3CR1 and Attenuating M1 Activation of Microglia in the Spinal Cord of Rats Using a Sciatic Chronic Constriction Injury Model.Frontiers in neuroscience · 2021Article
- Glial Cell Line-Derived Neurotrophic Factor Family Ligands, Players at the Interface of Neuroinflammation and Neuroprotection: Focus Onto the Glia.Frontiers in cellular neuroscience · 2021Review
- Chemokine Signaling in Chemotherapy-Induced Neuropathic Pain.International journal of molecular sciences · 2019Review
- Involvement of Interleukin-10 in Analgesia of Electroacupuncture on Incision Pain.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- Histamine Excites Rat GABAergic Ventral Pallidum Neurons via Co-activation of H1 and H2 Receptors.Neuroscience bulletin · 2018Article
- Recent Progress in Understanding the Mechanisms of Pain and Itch: the Second Special Issue.Neuroscience bulletin · 2018Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tetanic stimulation of the sciatic nerve (TSS) triggers long-term potentiation in the dorsal horn of the spinal cord and long-lasting pain hypersensitivity. CX3CL1-CX3CR1 signaling is an important pathway in neuronal-microglial activation. Nuclear factor κB (NF-κB) is a key signal transduction molecule that regulates neuroinflammation and neuropathic pain. Here, we set out to determine whether and how NF-κB and CX3CR1 are involved in the mechanism underlying the pathological changes induced by TSS. After unilateral TSS, significant bilateral mechanical allodynia was induced, as assessed by the von Frey test. The expression of phosphorylated NF-κB (pNF-κB) and CX3CR1 was significantly up-regulated in the bilateral dorsal horn. Immunofluorescence staining demonstrated that pNF-κB and NeuN co-existed, implying that the NF-κB pathway is predominantly activated in neurons following TSS. Administration of either the NF-κB inhibitor ammonium pyrrolidine dithiocarbamate or a CX3CR1-neutralizing antibody blocked the development and maintenance of neuropathic pain. In addition, blockade of NF-κB down-regulated the expression of CX3CL1-CX3CR1 signaling, and conversely the CX3CR1-neutralizing antibody also down-regulated pNF-κB. These findings suggest an involvement of NF-κB and the CX3CR1 signaling network in the development and maintenance of TSS-induced mechanical allodynia. Our work suggests the potential clinical application of NF-κB inhibitors or CX3CR1-neutralizing antibodies in treating pathological pain.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.