ArticleScientific reports2015
Hydrogen sulfide-induced itch requires activation of Cav3.2 T-type calcium channel in mice.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- Transdermal Hydrogen Sulfide Delivery Enabled by Open-Metal-Site Metal-Organic Frameworks.Journal of the American Chemical Society · 2024Article
- Beneficial Effects of Two Hydrogen Sulfide (HPharmaceutics · 2023Article
- Cardiac vagal afferent neurotransmission in health and disease: review and knowledge gaps.Frontiers in neuroscience · 2023Review
- Melatonin attenuates acute and chronic itch in mice: the antioxidant and anti-inflammatory effects of melatonin receptors.Annals of translational medicine · 2022Article
- Study of the Involvement of the P2Y12 Receptor in Chronic Itching in Type 2 Diabetes Mellitus.Molecular neurobiology · 2022Article
- Ethosuximide inhibits acute histamine- and chloroquine-induced scratching behavior in mice.Molecular brain · 2021Article
- Hydrogen sulfide: Recent progress and perspectives for the treatment of dermatological diseases.Journal of advanced research · 2021Review
- Thermal Hyperalgesia and Mechanical Allodynia Elicited by Histamine and Non-histaminergic Itch Mediators: Respective Involvement of TRPV1 and TRPA1.Neuroscience · 2020Article
- Cav3.2 T-type calcium channels control acute itch in mice.Molecular brain · 2020Article
- New insights into the mechanisms behind mechanical itch.Experimental dermatology · 2020Article
- Capsaicin-Sensitive Sensory Nerves and the TRPV1 Ion Channel in Cardiac Physiology and Pathologies.International journal of molecular sciences · 2020Review
- Hydrogen sulfide and dermatological diseases.British journal of pharmacology · 2020Review
- KLHL1 Controls CaFrontiers in molecular neuroscience · 2019Article
- The role of NaTheranostics · 2019Article
- A common haplotype containing functional CACNA1H variants is frequently coinherited with increased TPSAB1 copy number.Genetics in medicine : official journal of the American College of Medical Genetics · 2018Article
- TNF-α/TNFR1 Signaling is Required for the Full Expression of Acute and Chronic Itch in Mice via Peripheral and Central Mechanisms.Neuroscience bulletin · 2018Article
- Antioxidants Attenuate Acute and Chronic Itch: Peripheral and Central Mechanisms of Oxidative Stress in Pruritus.Neuroscience bulletin · 2017Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The contributions of gasotransmitters to itch sensation are largely unknown. In this study, we aimed to investigate the roles of hydrogen sulfide (H2S), a ubiquitous gasotransmitter, in itch signaling. We found that intradermal injection of H2S donors NaHS or Na2S, but not GYY4137 (a slow-releasing H2S donor), dose-dependently induced scratching behavior in a μ-opioid receptor-dependent and histamine-independent manner in mice. Interestingly, NaHS induced itch via unique mechanisms that involved capsaicin-insensitive A-fibers, but not TRPV1-expressing C-fibers that are traditionally considered for mediating itch, revealed by depletion of TRPV1-expressing C-fibers by systemic resiniferatoxin treatment. Moreover, local application of capsaizapine (TRPV1 blocker) or HC-030031 (TRPA1 blocker) had no effects on NaHS-evoked scratching. Strikingly, pharmacological blockade and silencing of Cav3.2 T-type calcium channel by mibefradil, ascorbic acid, zinc chloride or Cav3.2 siRNA dramatically decreased NaHS-evoked scratching. NaHS induced robust alloknesis (touch-evoked itch), which was inhibited by T-type calcium channels blocker mibefradil. Compound 48/80-induced itch was enhanced by an endogenous precursor of H2S (L-cysteine) but attenuated by inhibitors of H2S-producing enzymes cystathionine γ-lyase and cystathionine β-synthase. These results indicated that H2S, as a novel nonhistaminergic itch mediator, may activates Cav3.2 T-type calcium channel, probably located at A-fibers, to induce scratching and alloknesis in mice.
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