IP3-Independent Release of Ca2+ From Intracellular Stores: A Novel Mechanism for Transduction of Bitter Stimuli

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dc.contributor.authorOgura, Tatsuya
dc.contributor.authorKinnamon, Sue C.
dc.date.accessioned2021-02-24T17:34:13Z
dc.date.available2021-02-24T17:34:13Z
dc.date.issued1999-11-01
dc.descriptionUMBC Weihong Lin Laben_US
dc.description.abstractA variety of substances with different chemical structures elicits a bitter taste. Several different transduction mechanisms underlie detection of bitter tastants; however, these have been described in detail for only a few compounds. In addition, most studies have focused on mammalian taste cells, of which only a small subset is responsive to any particular bitter compound. In contrast, ∼80% of the taste cells in the mudpuppy, Necturus maculosus, are bitter-responsive. In this study, we used Ca²⁺ imaging and giga-seal whole cell recording to compare the transduction of dextromethorphan (DEX), a bitter antitussive, with transduction of the well-studied bitter compound denatonium. Bath perfusion of DEX (2.5 mM) increased the intracellular Ca²⁺ level in most taste cells. The DEX-induced Ca²⁺ increase was inhibited by thapsigargin, an inhibitor of Ca²⁺ transport into intracellular stores, but not by U73122, an inhibitor of phospholipase C, or by ryanodine, an inhibitor of ryanodine-sensitive Ca²⁺ stores. Increasing intracellular cAMP levels with a cell-permeant cAMP analogue and a phosphodiesterase inhibitor enhanced the DEX-induced Ca²⁺ increase, which was inhibited partially by H89, a protein kinase A inhibitor. Electrophysiological measurements showed that DEX depolarized the membrane potential and inhibited voltage-gated Na+ and K+ currents in the presence of GDP-β-S, a blocker of G-protein activation. DEX also inhibited voltage-gated Ca²⁺ channels. We suggest that DEX, like quinine, depolarizes taste cells by block of voltage-gated K channels, which are localized to the apical membrane in mudpuppy. In addition, DEX causes release of Ca²⁺ from intracellular stores by a phospholipase C-independent mechanism. We speculate that the membrane-permeant DEX may enter taste cells and interact directly with Ca²+ stores. Comparing transduction of DEX with that of denatonium, both compounds release Ca²⁺ from intracellular stores. However, denatonium requires activation of phospholipase C, and the mechanism results in a hyperpolarization rather than a depolarization of the membrane potential. These data support the hypothesis that single taste receptor cells can use multiple mechanisms for transducing the same bitter compound.en_US
dc.description.sponsorshipWe thank Dr. Sandra L. Nelson for helpful discussions and Drs. Thomas Finger and Diego Restrepo for helpful comments on the manuscript. This work was supported by National Institute of Deafness and Other Communication Disorders Grants DC-00244 and DC-00766 and by a grant from the Procter & Gamble Co.en_US
dc.description.urihttps://journals.physiology.org/doi/full/10.1152/jn.1999.82.5.2657en_US
dc.format.extent10 pagesen_US
dc.genrejournal artilclesen_US
dc.identifierdoi:10.13016/m21u15-vzfz
dc.identifier.citationTatsuya Ogura, and Sue C. Kinnamon,IP3-Independent Release of Ca2+ From Intracellular Stores: A Novel Mechanism for Transduction of Bitter Stimuli, JNP, Vol. 82, No. 5, DOI: https://doi.org/10.1152/jn.1999.82.5.2657en_US
dc.identifier.urihttps://doi.org/10.1152/jn.1999.82.5.2657
dc.identifier.urihttp://hdl.handle.net/11603/21076
dc.language.isoen_USen_US
dc.publisherAmerican Physiological Society (APS)en_US
dc.relation.isAvailableAtThe University of Maryland, Baltimore County (UMBC)
dc.relation.ispartofUMBC Biological Sciences Department Collection
dc.rightsThis item is likely protected under Title 17 of the U.S. Copyright Law. Unless on a Creative Commons license, for uses protected by Copyright Law, contact the copyright holder or the author.
dc.subjectbitter tasteen_US
dc.subjectmammalian taste cellsen_US
dc.subjectbitter responsiveen_US
dc.subjecttransduction mechanismsen_US
dc.titleIP3-Independent Release of Ca2+ From Intracellular Stores: A Novel Mechanism for Transduction of Bitter Stimulien_US
dc.typeTexten_US

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