Capsaicin modulates K+ currents from dissociated rat taste receptor cells.

Chili pepper is one of most widely used spices. The main active component of chili pepper is the capsaicin. The effects of capsaicin on sensory nerve endings are well known; however, little is known regarding the direct effect of capsaicin on taste receptor cells (TRCs). In this study, patch clamp methods were used to study the effects of capsaicin on the K(+) currents in TRCs isolated from the rat circumvallate papilla. Fura-2 microspectrofluorimetry was also used to determine the effects of capsaicin on the intracellular Ca(2+) concentration ([Ca(2+)](i)). In the resting state, whole-cell experiments identified outward-rectifying K(+) currents, which were inhibited by 5 mM tetraethylammonium (TEA(+)) chloride. Voltage-dependent K(+) channels with a conductance of 55+/-4 pS (mean+/-S.E.M.; n=3), were observed in cell-attached patches. Capsaicin (500 nM) completely inhibited the outward-rectifying K(+) current in the whole-cell recordings. In cell-attached patches 500 nM capsaicin significantly reduced the open probability (P(o)) of the K(+) channels from 0.401+/-0.052 (n=3) in the resting state, to 0.018+/-0.002 (n=3, P<0.05 by unpaired t-test). In the fura-2-loaded TRCs, micromolar concentrations of capsaicin increased [Ca(2+)](i) in a dose-dependent manner, e.g., 100 microM capsaicin consistently increased the 340:380 fluorescence ratio from 1.04+/-0.05 in the resting state to 1.40+/-0.05 (n=28). These results suggest that capsaicin can enhance or modify the gustatory sensation by inhibiting the K(+) currents of the TRCs directly.