抄録
To clarify the involvement of G protein in denatonium signal transduction, we carried out a whole-cell patch-clamp analysis with isolated taste cells in mice. Two different responses were observed by applying GDP-β-S, a G-protein inhibitor. One response to denatonium was reduced by GDP-β-S (G-protein-dependent), whereas the other was not affected (G-protein-independent). These different patterns were also observed by concurrently inhibiting the phospholipase C β2 and phosphodiesterase pathways via G protein. These data suggest dual, G-protein-dependent and -independent mechanisms for denatonium. Moreover, the denatonium responses were not attenuated by singly inhibiting the phospholipase C β2 or phosphodiesterase pathway, implying that both pathways were involved in G-protein-dependent transduction. In the G-protein-independent cells, the response was abolished by the depletion of calcium ions within the intracellular store. These results suggest that Ca2+ release from the intracellular store is an important factor. Our data demonstrate multiple transduction pathways for denatonium in mammalian taste cells.
