ArticleProceedings of the National Academy of Sciences of the United States of America2015
Pain-enhancing mechanism through interaction between TRPV1 and anoctamin 1 in sensory neurons.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed, 157 citations in OpenAlex.
- Human heat sensation: A randomized crossover trial.Science advances · 2024Trial
- Infantile Pain Episodes Associated with Novel Nav1.9 Mutations in Familial Episodic Pain Syndrome in Japanese Families.PloS one · 2016Trial
- From Inflammation to Neuroplasticity: Molecular Mechanisms of Pain in Acute, Recurrent and Chronic Pancreatitis.International journal of molecular sciences · 2026Review
- Involvement of interaction between TRPM2 and IKCA1 in temperature-dependent movement and IL-1β production in mouse microglia.The journal of physiological sciences : JPS · 2026Article
- Targeting Microglia-Neuron Crosstalk to Regulate Neuronal Excitability: Novel Translational Approaches for Chronic Pain Intervention.International journal of molecular sciences · 2026Review
- ER stress-induced ITPR1/ANO1 signaling drives trigeminal neuropathic pain through calcium-dependent neuronal hyperexcitability.The journal of headache and pain · 2025Article
- Evaluation of the Effects of Eye Drops for Dry Eyes on Neuronal Pain Receptors in a Primary Culture Model of Trigeminal Ganglion Cells.Journal of clinical medicine · 2025Article
- Phytochemical Modulators of Nociception: A Review of Cannabis Terpenes in Chronic Pain Syndromes.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Multiple cAMP/PKA complexes at the STIM1 ER/PM junction specified by E-Syt1 and E-Syt2 reciprocally gates ANO1 (TMEM16A) via CaNature communications · 2025Article
- Calcium-activated ion channels drive atypical inhibition in medial habenula neurons.Science advances · 2025Article
- Regulatory Action of Calcium and Calcium Channels in Pain Pathways.International journal of biological sciences · 2025Review
- Implications of mechanosensitive ion channels in the pathogenesis of osteoarthritis: a comprehensive review.Frontiers in cell and developmental biology · 2025Review
- ANO1: central role and clinical significance in non-neoplastic and neoplastic diseases.Frontiers in immunology · 2025Review
- TRPV1: The key bridge in neuroimmune interactions.Journal of intensive medicine · 2024Review
- Article
- The tether function of the anoctamins.Cell calcium · 2024Review
- Niclosamide potentiates TMEM16A and induces vasoconstriction.The Journal of general physiology · 2024Article
- Inhibition of mucus secretion by niclosamide and benzbromarone in airways and intestine.Scientific reports · 2024Article
- Thermosensation and TRP Channels.Advances in experimental medicine and biology · 2024Review
- Function and Regulation of the Calcium-Activated Chloride Channel Anoctamin 1 (TMEM16A).Handbook of experimental pharmacology · 2024Article
33 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The capsaicin receptor transient receptor potential cation channel vanilloid 1 (TRPV1) is activated by various noxious stimuli, and the stimuli are converted into electrical signals in primary sensory neurons. It is believed that cation influx through TRPV1 causes depolarization, leading to the activation of voltage-gated sodium channels, followed by the generation of action potential. Here we report that the capsaicin-evoked action potential could be induced by two components: a cation influx-mediated depolarization caused by TRPV1 activation and a subsequent anion efflux-mediated depolarization via activation of anoctamin 1 (ANO1), a calcium-activated chloride channel, resulting from the entry of calcium through TRPV1. The interaction between TRPV1 and ANO1 is based on their physical binding. Capsaicin activated the chloride currents in an extracellular calcium-dependent manner in HEK293T cells expressing TRPV1 and ANO1. Similarly, in mouse dorsal root ganglion neurons, capsaicin-activated inward currents were inhibited significantly by a specific ANO1 antagonist, T16Ainh-A01 (A01), in the presence of a high concentration of EGTA but not in the presence of BAPTA [1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid]. The generation of a capsaicin-evoked action potential also was inhibited by A01. Furthermore, pain-related behaviors in mice treated with capsaicin, but not with αβ-methylene ATP, were reduced significantly by the concomitant administration of A01. These results indicate that TRPV1-ANO1 interaction is a significant pain-enhancing mechanism in the peripheral nervous system.
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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.