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J Neurophysiol. 2008 Mar;99(3):1503-14. doi: 10.1152/jn.00892.2007. Epub 2008 Jan 16.

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

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Dept. of Biological Sciences, Univ. at Buffalo, The State University of New York, Buffalo, NY 14260, USA.


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 PLCbeta2 knock-out animals, indicating that the perception of these stimuli depends solely on PLCbeta2. In contrast, another study found that PLCbeta2 knock-out mice have a reduced, but not abolished, capacity to detect these taste qualities, suggesting a PLCbeta2-independent signaling pathway may be involved in the detection of taste stimuli. Since PLCbeta2-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 PLCbeta3 and IP(3)R1, indicating the presence of multiple PLC signaling pathways in taste cells.

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