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J Neurophysiol 91: 1297-1313, 2004. First published November 5, 2003; doi:10.1152/jn.00809.2003
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Na+-H+ Exchange Activity in Taste Receptor Cells

Anna K. Vinnikova1, Rammy I. Alam2, Shahbaz A. Malik2, Glenn L. Ereso2, George M. Feldman1,2,3, John M. McCarty1,3, Mark A. Knepper4, Gerard L. Heck2, John A. DeSimone2 and Vijay Lyall2

1Department of Internal Medicine and 2Department of Physiology, Virginia Commonwealth University, Richmond 23298; 3McGuire Veterans Affairs Medical Center, Richmond, Virginia 23249; and 4National Institutes of Health, Bethesda, Maryland 20892-1603

Submitted 20 August 2003; accepted in final form 29 October 2003

mRNA for two Na+-H+-exchanger isoforms 1 and 3 (NHE-1 and NHE-3) was detected by RT-PCR in fungiform and circumvallate taste receptor cells (TRCs). Anti-NHE-1 antibody binding was localized to the basolateral membranes, and the anti-NHE-3 antibody was localized in the apical membranes of fungiform and circumvallate TRCs. In a subset of TRCs, NHE-3 immunoreactivity was also detected in the intracellular compartment. For functional studies, an isolated lingual epithelium containing a single fungiform papilla was mounted with apical and basolateral sides isolated and perfused with nominally CO2/HCO3--free physiological media (pH 7.4). The TRCs were monitored for changes in intracellular pH (pHi) and Na+ ([Na+]i) using fluorescence ratio imaging. At constant external pH, 1) removal of basolateral Na+ reversibly decreased pHi and [Na+]i; 2) HOE642, a specific blocker, and amiloride, a nonspecific blocker of basolateral NHE-1, attenuated the decrease in pHi and [Na+]i; 3) exposure of TRCs to basolateral NH4Cl or sodium acetate pulses induced transient decreases in pHi that recovered spontaneously to baseline; 4) pHi recovery was inhibited by basolateral amiloride, 5-(N-methyl-N-isobutyl)-amiloride (MIA), 5-(N-ethyl-N-isopropyl)-amiloride (EIPA), HOE642, and by Na+ removal; 5) HOE642, MIA, EIPA, and amiloride inhibited pHi recovery with Ki values of 0.23, 0.46, 0.84, and 29 µM, respectively; and 6) a decrease in apical or basolateral pH acidified TRC pHi and inhibited spontaneous pHi recovery. The results indicate the presence of a functional NHE-1 in the basolateral membranes of TRCs. We hypothesize that NHE-1 is involved in sour taste transduction since its activity is modulated during acid stimulation.

Address for reprint requests and other correspondence: V. Lyall, Dept. of Physiology, Virginia Commonwealth Univ., Sanger Hall 3002, 1101 E. Marshall St., Richmond, VA 23298-0551 (E-mail: vlyall{at}hsc.vcu.edu).




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