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- W4319880470 abstract "Transient receptor potential vanilloid 1 (TRPV1) is expressed predominantly in peripheral nociceptors integrating diverse noxious stimuli. Activation of TRPV1 leads to a cascade of pro-nociceptive mechanisms, particularly, TRPV1 activation can inhibit the slow activating KCNQ2/3 current, the inhibition apparently depends on the A-kinase anchoring protein 5 (AKAP5) expression, forming a pro-nociceptive multiprotein complex. Eugenol is an aromatic oil extracted from cloves and widely used for dental pain treatment. It features multiple functions and regulate diverse ion channels. By using electrophysiological recordings on HEK293 cells, we show that eugenol is a weak activator of the TRPV1 but functions as an antagonist because it competes with capsaicin for the same binding pocket attenuating the TRPV1 current. Eugenol also serves as an activator of the KCNQ2/3 channels, shifting the voltage-dependent activation to negative voltages (−15 mV) and accelerating the activation kinetics by >3 fold. Eugenol does not show preference for KCNQ2 or KCNQ3. In cells expressing the multiprotein complex, application of a low concentration of capsaicin (100 nM) for 5 minutes, reproduces the TRPV1-dependent inhibition of KCNQ2/3, but it is prevented by the presence of high concentrations of eugenol. These data suggests that eugenol provides an inhibitory control for noxious stimuli in sensory neurons, by antagonizing TRPV1 and lowering the activation threshold of KCNQ2/3, silencing the neurons." @default.
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- W4319880470 date "2023-02-01" @default.
- W4319880470 modified "2023-09-26" @default.
- W4319880470 title "Eugenol rescues the TRPV1-dependent inhibition of KCNQ2/3" @default.
- W4319880470 doi "https://doi.org/10.1016/j.bpj.2022.11.2724" @default.
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