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- W2067085911 abstract "The antifungal and amoebicidal drug clioquinol (CQ) was withdrawn from the market when it was linked to an epidemic of subacute myelo-optico-neuropathy (SMON). Clioquinol exerts its anti-parasitic actions by acting as a Cu/Zn chelator and ionophore. Here we show that local injections of CQ produce mechanical hyperalgesia and cold hypersensitivity through a mechanism involving TRPA1 in mice. We also show that CQ activates TRPA1 in a Zn(2+)-dependent manner. Using a different Zn(2+)-ionophore, zinc pyrithione (ZnPy), we demonstrate that low, nanomolar concentrations of intracellular Zn(2+) ([Zn(2+)](i)) stimulate TRPA1. Direct application of Zn(2+) to the intracellular face of excised, inside-out patches activates TRPA1 with an EC(50) value of 7.5 +/- 1 nM. TRPA1 is expressed in a subpopulation of nociceptive dorsal root ganglion (DRG) neurons, where it acts as a sensory receptor for environmental irritants and oxidants. Using cultured DRG neurons from wild-type and TRPA1-deficient mice, we demonstrate that TRPA1 is the principal excitatory receptor for increased [Zn(2+)](i) in DRG neurons. In conclusion, we have discovered that TRPA1 acts a sensor of intracellular Zn(2+), and that Zn(2+) ionophores, such as CQ and ZnPy, activate TRPA1 by increasing [Zn(2+)](i). We also demonstrate that CQ-evoked mechanical hyperalgesia and cold allodynia require TRPA1 in vivo." @default.
- W2067085911 created "2016-06-24" @default.
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- W2067085911 date "2009-05-19" @default.
- W2067085911 modified "2023-10-07" @default.
- W2067085911 title "Clioquinol and pyrithione activate TRPA1 by increasing intracellular Zn <sup>2+</sup>" @default.
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- W2067085911 doi "https://doi.org/10.1073/pnas.0812675106" @default.
- W2067085911 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2688854" @default.
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