Journal
JOURNAL OF NEUROPHYSIOLOGY
Volume 87, Issue 6, Pages 3152-3155Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/jn.2002.87.6.3152
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- NIDCD NIH HHS [DC-03155, DC-00766, DC-00244, DC-03055] Funding Source: Medline
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Previous studies in rat and mouse have shown that brief exposure to the bitter stimulus denatonium induces an increase in [Ca2+](i) due to Ca2+ release from intracellular Ca2+ stores, rather than Ca2+ influx. We report here that prolonged exposure to denatonium induces sustained increases in [Ca2+](i) that are dependent on Ca2+ influx. Similar results were obtained from taste cells of the mud-puppy, Necturus maculosus, as well as green fluorescent protein (GFP) tagged gustducin-expressing taste cells of transgenic mice. In a subset of mudpuppy taste cells, prolonged exposure to denatonium induced oscillatory Ca2+ responses. Depletion of Ca2+ stores by thapsigargin also induced Ca2+ influx, suggesting that Ca2+ store-operated channels (SOCs) are present in both mudpuppy taste cells and gustducin-expressing taste cells of mouse. Further, treatment with thapsigargin prevented subsequent responses to denatonium, suggesting that the SOCs were the source of the Ca2+ influx. These data suggest that SOCs may contribute to bitter taste transduction and to regulation of Ca2+ homeostasis in taste cells.
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