Evidence for two populations of bitter responsive taste cells in mice.

Taste receptor cells use multiple signaling mechanisms to detect different taste stimuli in the oral cavity. Ionic stimuli (sour, salty) interact directly with ion channels to elicit responses, whereas bitter, sweet, and umami tastants activate G protein-coupled receptors to initiate phospholipase C (PLC)-dependent release of calcium from intracellular stores. However, the precise role for PLC in taste responses remains unclear. One study reported that bitter, sweet, and umami detection is abolished in PLC beta 2 knockout animals, indicating that the perception of these stimuli depends solely on PLC beta 2. In contrast, another study found that PLC beta 2 knock-out mice have a reduced, but not abolished, capacity to detect these taste qualities, suggesting a PLC beta 2-independent signaling pathway may be involved in the detection of taste stimuli. Since PLC beta 2-expressing taste cells do not have conventional synapses or express voltage-gated calcium channels (VGCCs), we sought to determine if any taste cells responding to bitter express VGCCs. We characterized calcium responses generated by bitter stimuli to activate the PLC pathway and 50 mM KCl to activate VGCCs. Comparisons of evoked calcium responses found that these two stimuli generated significantly different responses. Surprisingly, although most responsive taste cells responded to bitter or 50 mM KCl, some taste cells responded to both. Analysis of dual responsive cells found that bitter responses were inhibited by the PLC inhibitor U73122. Immunocytochemical analysis detected PLC beta 3 and IP(3)R1, indicating the presence of multiple PLC signaling pathways in taste cells.