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 while 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 reports that bitter, sweet and umami detection is abolished in PLC2 knock-out animals, indicating that the perception of these stimuli depends solely on PLC2 (Zhang et al. 2003). In contrast, another study found that PLC2 knock-out mice have a reduced but not abolished, capacity to detect these taste qualities (Dotson et al. 2005) suggesting a PLC2 -independent signaling pathway may be involved in the detection of taste stimuli. Since PLC2-expressing taste cells do not have conventional synapses or express voltage-gated calcium channels (VGCCs) (Clapp et al. 2006; DeFazio et al. 2006), 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 50mM KCl to activate VGCCs. Comparisons of evoked calcium responses found that these two stimuli generated significantly different responses. Surprisingly, while most responsive taste cells responded to bitter or 50mM 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 PLC3 and IP₃R1, indicating the presence of multiple PLC signaling pathways in taste cells.