Taste receptor cell responses to the bitter stimulus denatonium involve Ca2+ influx via store-operated channels

J Neurophysiol. 2002 Jun;87(6):3152-5. doi: 10.1152/jn.2002.87.6.3152.


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 mudpuppy, 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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Calcium / pharmacology
  • Calcium Channels / physiology*
  • Enzyme Inhibitors / pharmacology
  • Gene Expression / physiology
  • Mice
  • Mice, Transgenic
  • Necturus
  • Quaternary Ammonium Compounds
  • Stimulation, Chemical
  • Taste / physiology*
  • Taste Buds / physiology*
  • Thapsigargin / pharmacology
  • Transducin / genetics


  • Calcium Channels
  • Enzyme Inhibitors
  • Quaternary Ammonium Compounds
  • denatonium chloride
  • gustducin
  • Thapsigargin
  • Transducin
  • Calcium