Sodium taste elicits ATP secretion in mouse taste buds (LB71)

Abstract

Taste buds contain two types of cells that directly participate in gustatory transduction‐‐ Receptor (Type II) and Presynaptic (Type III) cells. Receptor cells respond to sweet, bitter and umami taste stimulation. Presynaptic cells have been identified with confidence as sour (acid) taste‐sensing cells. Using confocal Ca2+ imaging in a lingual slice preparation, Tomchik et al. (2007) showed that some vallate taste cells responded to salt (Na+) taste. Recently, ion channels (ENaC) believed to underlie salt taste transduction were reported to be in taste cells that were neither Receptor (Type II) or Presynaptic (Type III) cells. Yet, mechanisms of Na+ taste transduction and the identity of the cells that respond to Na+ stimulation remain controversial. Using Ca2+ imaging on isolated mouse vallate taste cells loaded with Fura 2, we demonstrate here that a subset of cells, neither Receptor nor Presynaptic cells, show Ca2+ mobilization in response to Na+ stimulation. Removing extracellular Ca2+ had no effect on responses evoked by Na+ stimulation. In marked contrast, applying 1 μM thapsigargin, a SER Ca‐ATPase inhibitor, or 10 μM U73122, a PLC blocker, eliminated Na+ responses, suggesting that Na+ stimulation triggers PLC/IP3‐mediated release of Ca2+ from intracellular stores. Next, we used CHO cells expressing P2X receptors as biosensors to monitor ATP release from taste buds and isolated taste cells. Na+ stimulation elicited robust biosensor responses that were blocked by suramin, confirming that Na+ stimulation elicits ATP secretion from taste buds/cells. Carbenoxolone (5 μM) or probenecid (250 μM), blockers of pannexin1 hemichannels, reversibly blocked Na‐evoked ATP secretion. Our data indicate that salt taste stimulus triggers a dedicated population of taste cells to secrete ATP via pannexin1hemmichannels.Grant Funding Source: Supported by SIUSOM and NIH/NIDCD DC007630