Basolateral Na + –H + exchanger‐1 in rat taste receptor cells is involved in neural adaptation to acidic stimuli

The role of basolateral Na + –H + exchanger isoform‐1 (NHE‐1) was investigated in neural adaptation of rat taste responses to acidic stimuli, by direct measurement of intracellular pH (pH i ) in polarized taste receptor cells (TRCs) and by chorda tympani (CT) taste nerve recordings. In TRCs perfused with CO 2 /HCO 3 − ‐free solution (pH 7.4), removal of basolateral Na + decreased pH i reversibly and zoniporide, a specific NHE‐1 blocker, inhibited the Na + ‐induced changes in pH i . The spontaneous rate of TRC pH i recovery from NH 4 Cl pulses was inhibited by basolateral zoniporide with a K i of 0.33μ m . Exposure to basolateral ionomycin, reversibly increased TRC Ca 2+ , resting pH i , and the spontaneous rate of pH i recovery from an NH 4 Cl pulse. These effects of Ca 2+ on pH i were blocked by zoniporide. In in vivo experiments, topical lingual application of zoniporide increased the magnitude of the CT responses to acetic acid and CO 2 , but not to HCl. Topical lingual application of ionomycin did not affect the phasic part of the CT responses to acidic stimuli, but decreased the tonic part by 50% of control over a period of about 1 min. This increased adaptation in the CT response was inhibited by zoniporide. Topical lingual application of 8‐CPT‐cAMP increased the CT responses to HCl, but not to CO 2 , and acetic acid. In the presence of cAMP, ionomycin increased sensory adaptation to HCl, CO 2 , and acetic acid. Thus, cAMP and Ca 2+ independently modulate CT responses to acidic stimuli. While cAMP enhances TRC apical H + entry and CT responses to strong acid, an increase in Ca 2+ activates NHE‐1, and increases neural adaptation to all acidic stimuli.