ArticleProceedings of the National Academy of Sciences of the United States of America2016
Inflammatory and neuropathic cold allodynia are selectively mediated by the neurotrophic factor receptor GFRα3.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed.
- Recombinant Artemin-Fc Fusion Protein Attenuates TLR4/NF-κB-Associated Neuroinflammation and Modulates Inhibitory/Excitatory Synaptic Marker Expression After Spinal Cord Injury.CNS neuroscience & therapeutics · 2026Article
- Identification of Biomarker in Kidney Stone Disease by Integrating Transcriptomics and Olink Proteomics: A Case-Control Study.Journal of inflammation research · 2026Article
- Artemin/GFRA3 axis and TRP channels: molecular insights from a feline model of osteoarthritis.Frontiers in pain research (Lausanne, Switzerland) · 2026Article
- Article
- Neuronal Endothelin a Receptor Mediates Experimental and Clinical Vascular Pain through an Endothelial-Neural Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Transduction Mechanisms for Cold Temperature in Mouse Trigeminal and Vagal Ganglion Neurons Innervating Different Peripheral Organs.Acta physiologica (Oxford, England) · 2025Article
- Emerging evidence of artemin/GFRα3 signaling in musculoskeletal pain.Osteoarthritis and cartilage · 2025Review
- Investigation of the Effect of Rose Oxide in Animal Models of Paclitaxel-induced Neuropathic Pain in Rats.Current pharmaceutical design · 2025Article
- The neurotrophic factor artemin and its receptor GFRα3 mediate migraine-like pain via the ion channel TRPM8.Cephalalgia : an international journal of headache · 2024Article
- Ion channels of cold transduction and transmission.The Journal of general physiology · 2024Review
- The neurotrophic factor artemin and its receptor GFRα3 mediate migraine-like pain via the ion channel TRPM8.bioRxiv : the preprint server for biology · 2024Article
- Article
- Phenytoin Decreases Pain-like Behaviors and Improves Opioid Analgesia in a Rat Model of Neuropathic Pain.Brain sciences · 2023Article
- Endogenous inflammatory mediators produced by injury activate TRPV1 and TRPA1 nociceptors to induce sexually dimorphic cold pain that is dependent on TRPM8 and GFRα3.bioRxiv : the preprint server for biology · 2023Article
- The transient receptor potential channels in rheumatoid arthritis: Need to pay more attention.Frontiers in immunology · 2023Review
- Immunoglobulin somatic hypermutation in a defined biochemical system recapitulates affinity maturation and permits antibody optimization.Nucleic acids research · 2022Article
- Analgesic effects of Terminalia chebula extract are mediated by the suppression of the protein expression of nerve growth factor and nuclear factor-κB in the brain and oxidative markers following neuropathic pain in rats.Molecular biology reports · 2022Article
- Anti-inflammatory potential of liraglutide, a glucagon-like peptide-1 receptor agonist, in rats with peripheral acute inflammation.Inflammopharmacology · 2022Article
- The distinctive role of menthol in pain and analgesia: Mechanisms, practices, and advances.Frontiers in molecular neuroscience · 2022Review
- Investigating the Role of Artemin and Its Cognate Receptor, GFRα3, in Osteoarthritis Pain.Frontiers in neuroscience · 2022Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Tissue injury prompts the release of a number of proalgesic molecules that induce acute and chronic pain by sensitizing pain-sensing neurons (nociceptors) to heat and mechanical stimuli. In contrast, many proalgesics have no effect on cold sensitivity or can inhibit cold-sensitive neurons and diminish cooling-mediated pain relief (analgesia). Nonetheless, cold pain (allodynia) is prevalent in many inflammatory and neuropathic pain settings, with little known of the mechanisms promoting pain vs. those dampening analgesia. Here, we show that cold allodynia induced by inflammation, nerve injury, and chemotherapeutics is abolished in mice lacking the neurotrophic factor receptor glial cell line-derived neurotrophic factor family of receptors-α3 (GFRα3). Furthermore, established cold allodynia is blocked in animals treated with neutralizing antibodies against the GFRα3 ligand, artemin. In contrast, heat and mechanical pain are unchanged, and results show that, in striking contrast to the redundant mechanisms sensitizing other modalities after an insult, cold allodynia is mediated exclusively by a single molecular pathway, suggesting that artemin-GFRα3 signaling can be targeted to selectively treat cold pain.
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