ArticleThe Journal of biological chemistry2013
Excitation and modulation of TRPA1, TRPV1, and TRPM8 channel-expressing sensory neurons by the pruritogen chloroquine.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 97 citations in OpenAlex.
- Electroacupuncture synergizes with anti-ferroptosis bioelectrical niche remodeling to promote spinal cord regeneration.Materials today. Bio · 2026Article
- Electroacupuncture reduces calcium influx and inhibits endoplasmic reticulum stress by inhibiting the PKCδ-TRPA1 pathway to promote motor function recovery after spinal cord injury.Burns & trauma · 2026Article
- Spinal TRPC3 promotes neuropathic pain and coordinates phospholipase C-induced mechanical hypersensitivity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Acetone-Ether-Water Mouse Model of Persistent Itch Fully Resolves Without Latent Pruritic or Cross-Modality Priming.Dermatopathology (Basel, Switzerland) · 2025Article
- Lysophosphatidic Acid Receptors LPAR5 and LPAR2 Inversely Control Hydroxychloroquine-Evoked Itch and Scratching in Mice.International journal of molecular sciences · 2024Article
- Calcitonin gene‑related peptide alleviates hyperoxia‑induced human alveolar cell injury via the CGRPR/TRPV1/Ca2Molecular medicine reports · 2024Article
- Characterization of human iPSC-derived sensory neurons and their functional assessment using multi electrode array.Scientific reports · 2024Article
- Cimifugin Relieves Histamine-Independent Itch in Atopic Dermatitis via Targeting the CQ Receptor MrgprA3.ACS omega · 2024Article
- MrgprA3-expressing pruriceptors drive pruritogen-induced alloknesis through mechanosensitive Piezo2 channel.Cell reports · 2023Article
- Medial and dorsal lateral septum involving social disruption stress-primed escalation in acid-induced writhes.Frontiers in molecular neuroscience · 2023Article
- Melatonin attenuates acute and chronic itch in mice: the antioxidant and anti-inflammatory effects of melatonin receptors.Annals of translational medicine · 2022Article
- Mitochondrial Reactive Oxygen Species Elicit Acute and Chronic Itch via Transient Receptor Potential Canonical 3 Activation in Mice.Neuroscience bulletin · 2022Article
- Role of TRP ion channels in pruritus.Neuroscience letters · 2022Review
- Therapeutic potential of TRPM8 antagonists in prostate cancer.Scientific reports · 2021Article
- A neuropeptide code for itch.Nature reviews. Neuroscience · 2021Review
- Article
- A high-content platform for physiological profiling and unbiased classification of individual neurons.Cell reports methods · 2021Article
- The signaling pathway and polymorphisms of Mrgprs.Neuroscience letters · 2021Review
- Inhibition of M/KFrontiers in molecular neuroscience · 2020Article
- Role of TRP channels in GAmerican journal of physiology. Lung cellular and molecular physiology · 2020Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The sensations of pain, itch, and cold often interact with each other. Pain inhibits itch, whereas cold inhibits both pain and itch. TRPV1 and TRPA1 channels transduce pain and itch, whereas TRPM8 transduces cold. The pruritogen chloroquine (CQ) was reported to excite TRPA1, leading to the sensation of itch. It is unclear how CQ excites and modulates TRPA1(+), TRPV1(+), and TRPM8(+) neurons and thus affects the sensations of pain, itch, and cold. Here, we show that only 43% of CQ-excited dorsal root ganglion neurons expressed TRPA1; as expected, the responses of these neurons were completely prevented by the TRPA1 antagonist HC-030031. The remaining 57% of CQ-excited neurons did not express TRPA1, and excitation was not prevented by either a TRPA1 or TRPV1 antagonist but was prevented by the general transient receptor potential canonical (TRPC) channel blocker BTP2 and the selective TRPC3 inhibitor Pyr3. Furthermore, CQ caused potent sensitization of TRPV1 in 51.9% of TRPV1(+) neurons and concomitant inhibition of TRPM8 in 48.8% of TRPM8(+) dorsal root ganglion neurons. Sensitization of TRPV1 is caused mainly by activation of the phospholipase C-PKC pathway following activation of the CQ receptor MrgprA3. By contrast, inhibition of TRPM8 is caused by a direct action of activated Gαq independent of the phospholipase C pathway. Our data suggest the involvement of the TRPC3 channel acting together with TRPA1 to mediate CQ-induced itch. CQ not only elicits itch by directly exciting itch-encoding neurons but also exerts previously unappreciated widespread actions on pain-, itch-, and cold-sensing neurons, leading to enhanced pain and itch.
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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.