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Published March 11, 2010 | Accepted Version + Supplemental Material
Journal Article Open

The cells and peripheral representation of sodium taste in mice


Salt taste in mammals can trigger two divergent behavioural responses. In general, concentrated saline solutions elicit robust behavioural aversion, whereas low concentrations of NaCl are typically attractive, particularly after sodium depletion. Notably, the attractive salt pathway is selectively responsive to sodium and inhibited by amiloride, whereas the aversive one functions as a non-selective detector for a wide range of salts. Because amiloride is a potent inhibitor of the epithelial sodium channel (ENaC), ENaC has been proposed to function as a component of the salt-taste-receptor system. Previously, we showed that four of the five basic taste qualities—sweet, sour, bitter and umami—are mediated by separate taste-receptor cells (TRCs) each tuned to a single taste modality, and wired to elicit stereotypical behavioural responses. Here we show that sodium sensing is also mediated by a dedicated population of TRCs. These taste cells express the epithelial sodium channel ENaC, and mediate behavioural attraction to NaCl. We genetically engineered mice lacking ENaCα in TRCs, and produced animals exhibiting a complete loss of salt attraction and sodium taste responses. Together, these studies substantiate independent cellular substrates for all five basic taste qualities, and validate the essential role of ENaC for sodium taste in mice.

Additional Information

© 2010 Macmillan Publishers Limited. Received 4 November 2009; Accepted 5 January 2010; Published online 27 January 2010. We thank W. Guo and A. Becker for generation and maintenance of mouse lines, and K. Scott and members of our laboratories for valuable comments. This research was supported in part by the intramural research program of the NIH, NIDCR (N.J.P.R.). C.S.Z. is an investigator of the Howard Hughes Medical Institute. Author Contributions: J.C. designed the study, carried out electrophysiological and expression studies, analysed data and wrote the paper; C.K. designed and carried out behavioural experiments and analysed expression in engineered and knockout mice; Y.O. designed and carried out calcium imaging experiments and analysed data; D.A.Y. carried out molecular studies and helped write the paper; E.H. provided essential reagents; N.J.P.R. and C.S.Z. designed the study, analysed data and wrote the paper. The authors declare competing financial interests. C.S.Z. is a scientific founder and scientific advisory board member of Senomyx.

Attached Files

Accepted Version - nihms-168779.pdf

Supplemental Material - nature08783-s1.pdf


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