Faculty Opinions recommendation of Sour taste stimuli evoke Ca2+ and pH responses in mouse taste cells.

Author(s):  
Frank Zufall
Keyword(s):  
1998 ◽  
Vol 80 (4) ◽  
pp. 1852-1859 ◽  
Author(s):  
Takenori Miyamoto ◽  
Rie Fujiyama ◽  
Yukio Okada ◽  
Toshihide Sato

Miyamoto, Takenori, Rie Fujiyama, Yukio Okada, and Toshihide Sato. Sour transduction involves activation of NPPB-sensitive conductance in mouse taste cells. J. Neurophysiol. 80: 1852–1859, 1998. We examined the sour taste transduction mechanism in the mouse by applying whole cell patch-clamp technique to nondissociated taste cells from the fungiform papillae. Localized stimulation with 0.5 M NaCl and 25 mM citric acid (pH 3.0) of the apical membrane enabled us to obtain responses from single taste cells under a quasi-natural condition. Of 28 taste cells examined, 11 cells (39%) responded to 0.5 M NaCl alone and 2 cells (7%) responded to 25 mM citric acid alone, indicating the presence of salty- and sour-specific taste cells. Ten cells (36%) responded to both NaCl and citric acid and 5 cells (18%) responded to neither salt nor citric acid. Amiloride reversibly suppressed NaCl-induced responses in mouse taste cells but not citric acid-induced responses. On the other hand, a Cl− channel blocker, 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), reversibly suppressed all the citric-acid-induced responses. Most of the NaCl-induced current responses displayed an inwardly rectifying property, whereas all the citric-acid-induced responses displayed an outwardly rectifying property. The reversal potential for NPPB-sensitive component in citric-acid-induced current responses was −2 ± 7 mV (mean ± SE, n = 4), which was close to the equilibrium potential of Cl− ( E Cl), whereas the reversal potential for NPPB-insensitive component was 34 ± 8 mV ( n = 4). The reversal potential of citric-acid-induced current responses (19 ± 8 mV, n = 4) was mostly present at the middle point between reversal potentials of NPPB-sensitive and -insensitive current components. In some taste cells, an inorganic cation channel blocker, Cd2+, suppressed citric-acid-induced responses, but an inorganic stretch-activated cation channel blocker, Gd3+, did not affect these responses. These results suggest that salt- and acid-induced responses were mediated by differential transduction mechanisms in mouse taste cells and that NPPB-sensitive Cl− channels play a more important role to sour taste transduction rather than amiloride-sensitive Na+ channels. However, the fact that the reversal potentials of citric-acid-induced responses had more positive than E Cl suggests that Ca2+ or H+ permeable and poorly selective cation channels, which should be amiloride insensitive, may be activated by citric acid.


PLoS ONE ◽  
2011 ◽  
Vol 6 (10) ◽  
pp. e25471 ◽  
Author(s):  
Yijen A. Huang ◽  
Elizabeth Pereira ◽  
Stephen D. Roper

2003 ◽  
Vol 547 (2) ◽  
pp. 475-483 ◽  
Author(s):  
T. A. Richter ◽  
A. Caicedo ◽  
S. D. Roper
Keyword(s):  

1997 ◽  
Vol 28 ◽  
pp. S233 ◽  
Author(s):  
Takenori Miyamoto ◽  
Rie Fujiyama ◽  
Yukio Okada ◽  
Toshihide Sato

2003 ◽  
Vol 90 (5) ◽  
pp. 3283-3294 ◽  
Author(s):  
Sergey G. Baryshnikov ◽  
Olga A. Rogachevskaja ◽  
Stanislav S. Kolesnikov

Evidence implicates a number of neuroactive substances and their receptors in mediating complex cell-to-cell communications in the taste bud. Recently, we found that ATP, a ubiquitous neurotransmitter/neuromodulator, mobilizes intracellular Ca2+ in taste cells by activating P2Y receptors. Here, P2Y receptor-cellular response coupling was characterized in detail using single cell ratio photometry and the inhibitory analysis. The sequence of underlying events was shown to include ATP-dependent activation of PLC, IP3 production, and IP3 receptor-mediated Ca2+ release followed by Ca2+ influx. Data obtained favor SOC channels rather than receptor-operated channels as a pathway for Ca2+ influx that accompanies Ca2+ release. Intracellular Ca2+ mobilized by ATP is apparently extruded by the plasma membrane Ca2+-ATPase, while a contribution of the Na+/Ca2+ exchange and other mechanisms of Ca2+ clearance is negligible. Cyclic AMP-dependent phosphorylation is likely to control a gain of the phosphoinositide cascade involved in ATP transduction. ATP-responsive taste cells are abundant in circumvallate, foliate, and fungiform papillae. Taken together, our observations point to a putative role for ATP as a neurotransmitter operative in the taste bud.


2010 ◽  
Vol 104 (1) ◽  
pp. 529-538 ◽  
Author(s):  
Steven A. Szebenyi ◽  
Agnieszka I. Laskowski ◽  
Kathryn F. Medler

Taste cells use multiple signaling mechanisms to generate appropriate cellular responses to discrete taste stimuli. Some taste stimuli activate G protein coupled receptors (GPCRs) that cause calcium release from intracellular stores while other stimuli depolarize taste cells to cause calcium influx through voltage-gated calcium channels (VGCCs). While the signaling mechanisms that initiate calcium signals have been described in taste cells, the calcium clearance mechanisms (CCMs) that contribute to the termination of these signals have not been identified. In this study, we used calcium imaging to define the role of sodium-calcium exchangers (NCXs) in the termination of evoked calcium responses. We found that NCXs regulate the calcium signals that rely on calcium influx at the plasma membrane but do not significantly contribute to the calcium signals that depend on calcium release from internal stores. Our data indicate that this selective regulation of calcium signals by NCXs is due primarily to their location in the cell rather than to the differences in cytosolic calcium loads. This is the first report to define the physiological role for any of the CCMs utilized by taste cells to regulate their evoked calcium responses.


1999 ◽  
Vol 81 (6) ◽  
pp. 3087-3091 ◽  
Author(s):  
Yuzo Ninomiya ◽  
Toshiaki Imoto ◽  
Tadataka Sugimura

Sweet taste responses of mouse chorda tympani neurons: existence of gurmarin-sensitive and -insensitive receptor components. Inhibitory effects of gurmarin (gur) on responses to sucrose and other sweeteners of single fibers of the chorda tympani nerve in C57BL mice were examined. Of 30 single fibers that strongly responded to 0.5 M sucrose but were not or to lesser extent responsive to 0.1 M NaCl, 0.01 M HCl, and 0.02 M quinine HCl (sucrose-best fibers), 16 fibers showed large suppression of responses to sucrose and other sweeteners by lingual treatment with 4.8 μM (∼20 μg/ml) gur (suppressed to 4–52% of control: gur-sensitive fibers), whereas the remaining 14 fibers showed no such gur inhibition (77–106% of control: gur-insensitive fibers). In gur-sensitive fibers, responses to sucrose inhibited by gur recovered to ∼70% of control responses after rinsing the tongue with 15 mM β-cyclodextrin and were almost abolished by further treatment with 2% pronase. In gur-insensitive fibers, sucrose responses were not inhibited by gur, but were largely suppressed by pronase. These results suggest existence of two different receptor components for sweeteners with different susceptibilities to gur in mouse taste cells, one gur sensitive and the other gur insensitive. Taste cells possessing each component may be specifically innervated by a particular type of chorda tympani neurons.


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