ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Artemin, a glial cell line-derived neurotrophic factor family member, induces TRPM8-dependent cold pain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 116 citations in OpenAlex.
- Transient Receptor Potential Melastatin 8 Plays a Key Role in Dextran Sulfate Sodium-Induced Murine Colitis via Regulating Extrinsic Sensory Neurons and Enteric Macrophage Secretory Activities.Neurogastroenterology and motility · 2026Article
- Article
- Artemin/GFRA3 axis and TRP channels: molecular insights from a feline model of osteoarthritis.Frontiers in pain research (Lausanne, Switzerland) · 2026Article
- Artemin sensitises mouse (Mus musculus) and naked mole-rat (Heterocephalus glaber) sensory neurons in vitro.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2025Article
- Activation of central and peripheral transient receptor potential melastatin 8 increases susceptibility to spreading depolarization and facilitates trigeminal neuroinflammation.The journal of headache and pain · 2025Article
- Emerging evidence of artemin/GFRα3 signaling in musculoskeletal pain.Osteoarthritis and cartilage · 2025Review
- TRPM8 Mutations Associated With Persistent Pain After Surgical Injury of Corneal Trigeminal Axons.Neurology. Genetics · 2024Article
- The neurotrophic factor artemin and its receptor GFRα3 mediate migraine-like pain via the ion channel TRPM8.Cephalalgia : an international journal of headache · 2024Article
- The neurotrophic factor artemin and its receptor GFRα3 mediate migraine-like pain via the ion channel TRPM8.bioRxiv : the preprint server for biology · 2024Article
- Targeting Nociceptive Neurons and Transient Receptor Potential Channels for the Treatment of Migraine.International journal of molecular sciences · 2023Review
- Review
- 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
- TRP channels: a journey towards a molecular understanding of pain.Nature reviews. Neuroscience · 2022Review
- Systemic, Intrathecal, and Intracerebroventricular Antihyperalgesic Effects of the Calcium Channel Blocker CTK 01512-2 Toxin in Persistent Pain Models.Molecular neurobiology · 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
- Transient Receptor Potential Channels in the Epithelial-to-Mesenchymal Transition.International journal of molecular sciences · 2021Review
- Serum artemin is not correlated with sensitivity within dogs with naturally occurring osteoarthritis pain.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic pain associated with injury or disease can result from dysfunction of sensory afferents whereby the threshold for activation of pain-sensing neurons (nociceptors) is lowered. Neurotrophic factors control nociceptor development and survival, but also induce sensitization through activation of their cognate receptors, attributable, in part, to the modulation of ion channel function. Thermal pain is mediated by channels of the transient receptor potential (TRP) family, including the cold and menthol receptor TRPM8. Although it has been shown that TRPM8 is involved in cold hypersensitivity, the molecular mechanisms underlying this pain modality are unknown. Using microarray analyses to identify mouse genes enriched in TRPM8 neurons, we found that the glial cell line-derived neurotrophic factor (GDNF) family receptor GFRα3 is expressed in a subpopulation of TRPM8 sensory neurons that have the neurochemical profile of cold nociceptors. Moreover, we found that artemin, the specific GFRα3 ligand that evokes heat hyperalgesia, robustly sensitized cold responses in a TRPM8-dependent manner in mice. In contrast, GFRα1 and GFRα2 are not coexpressed with TRPM8 and their respective ligands GDNF and neurturin did not induce cold pain, whereas they did evoke heat hyperalgesia. Nerve growth factor induced mild cold sensitization, consistent with TrkA expression in TRPM8 neurons. However, bradykinin failed to alter cold sensitivity even though its receptor expresses in a subset of TRPM8 neurons. These results show for the first time that only select neurotrophic factors induce cold sensitization through TRPM8 in vivo, unlike the broad range of proalgesic agents capable of promoting heat hyperalgesia.
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Registered trials
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.