Sour transduction involves activation of NPPB-sensitive conductance in mouse taste cells.
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- (ECl), 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 ECl suggests that Ca2+ or H+ permeable and poorly selective cation channels, which should be amiloride insensitive, may be activated by citric acid.
Department of Physiology, Nagasaki University School of Dentistry, Nagasaki 852-8588, Japan.
T
T
Miyamoto
R
R
Fujiyama
Y
Y
Okada
T
T
Sato
D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D019343:Citric Acid / Q000037:antagonists & inhibitors / Q000494:pharmacology; D004553:Electric Conductivity; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D009431:Neural Conduction / Q000187:drug effects*; D009579:Nitrobenzoates / Q000494:pharmacology*; D015398:Signal Transduction / Q000502:physiology*; D012965:Sodium Chloride / Q000494:pharmacology; D013649:Taste / Q000502:physiology*; D013650:Taste Buds / Q000166:cytology / Q000187:drug effects / Q000502:physiology*
D009579:Nitrobenzoates; D019343:Citric Acid; C058176:5-nitro-2-(3-phenylpropylamino)benzoic acid; D012965:Sodium Chloride; D000584:Amiloride