Author(s): Kwak J
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Abstract Capsaicin, the pungent ingredient in hot pepper, activates nociceptors to produce pain and inflammation. However, prolonged exposures of capsaicin will cause desensitization to nociceptive stimuli. Hyperpolarization-activated cation currents (I(h)) contribute to the maintenance of the resting membrane potential and excitability of neurons. In the cultured dorsal root ganglion (DRG) neurons, we investigated mechanisms underlying capsaicin-mediated modulation of I(h) using patch clamp recordings. Capsaicin (1 µM) inhibited I(h) only in the capsaicin-sensitive neurons. The capsaicin-induced inhibition of I(h) was prevented by preexposing the TRPV1 antagonist, capsazepine (CPZ). Capsaicin-induced inhibition of I(h) was dose dependent (IC(50)= 0.68 µM) and partially abolished by intracellular BAPTA and cyclosporin A, specific calcineurin inhibitor. In summary, the inhibitory effects of capsaicin on I(h) are mediated by activation of TRPV1 and Ca(2+)-triggered cellular responses. Analgesic effects of capsaicin have been thought to be related to desensitization of nociceptive neurons due to depletion of pain-related substances. In addition, capsaicin-induced inhibition of I(h) is likely to be important in understanding the analgesic mechanism of capsaicin.
This article was published in Exp Neurobiol
and referenced in Alternative & Integrative Medicine