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The Journal of Neurophysiology Vol. 87 No. 6 June 2002, pp. 3152-3155
Copyright ©2002 by the American Physiological Society
RAPID COMMUNICATION
1Department of Anatomy and Neurobiology, Colorado State University, Fort Collins, Colorado 80523; 2Howard Hughes Medical Institute and Department of Physiology and Biophysics, Mount Sinai School of Medicine of New York University, New York, New York 10029; and 3Rocky Mountain Taste and Smell Center, University of Colorado Health Sciences Center, Denver, Colorado 80262
Ogura, Tatsuya,
Robert F. Margolskee, and
Sue C. Kinnamon.
Taste Receptor Cell Responses to the Bitter Stimulus Denatonium
Involve Ca2+ Influx Via Store-Operated Channels. J. Neurophysiol. 87: 3152-3155, 2002. 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.
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