The calcium-activated chloride  channels TMEM16A and TMEM16B play relevant roles in many physiological processes including neuronal excitability and regulation of Cl- homeostasis. We examined the presence of calcium-activated chloride channels in taste cells of mouse vallate papillae. Taste buds contain three main types of taste cells named type I, II or III. Type II and type III cells express taste receptors and respond to tastants, while type I cells mainly have glial-like functions. The three cell types can be identified by the expression of specific proteins and by their electrophysiological fingerprint. Previous work has shown that both TMEM16A and TMEM16B were expressed in taste cells (Cherkashin et al., 2016). We used Tmem16a and Tmem16b KO mice models as a control for the specificity of antibodies and found that only TMEM16A, but not TMEM16B, was expressed in taste bud cells. Moreover, TMEM16A largely colocalized with the inwardly rectifier K+ channel KCNJ1 at the apical portion of type I cells. By using whole-cell patch-clamp recordings in isolated cells from taste buds, we measured large currents activated by 1.5 μM Ca2+ in the intracellular solution in type I, but not in type II and III taste bud cells. Ion substitution experiments indicated that the current was mainly carried by anions. Calcium-activated chloride currents were blocked by the specific TMEM16A channel blocker Ani9. Moreover, in agreement with previous studies showing that type I taste cells exhibited large Ca2+-activated Cl- currents when stimulated with P2Y receptor agonists (Kim et al. 2000; Cherkashin et al. (2016), we found that 50 μM ATP at the holding potential of -70 mV induced large inward currents in about 70% of type I taste cells. These currents were blocked by Ani9, indicating a possible role of TMEM16A in ATP-mediated signaling. ATP is released by type II cells in response to various tastants and reaches type I cells where it is hydrolyzed by ecto-ATPases but can also increase cytolosic Ca2+ by binding to P2Y receptors and indirectly activate TMEM16A channels causing a flux of Cl− according to its electrochemical gradient.