A psychophysical and electrophysiological analysis of salt taste in Trpv1 null mice

Current evidence suggests salt taste transduction involves at least two mechanisms, one that is amiloride sensitive and appears to use apically located epithelial sodium channels relatively selective for Na(+) and a second that is amiloride insensitive and uses a variant of the transient receptor potential vanilloid receptor I (TRPVI) that serves as a nonspecific cation channel. To provide a functional context for these findings, we trained Trpvl knockout (KO) and wild-type (WT) C57BL/6J mice (n = 9 or 10/group) in a two-response operant discrimination procedure and measured detection thresholds to NaCl and KCl with and without amiloride. The KO and WT mice had similar detection thresholds for NaCl and KCl. Amiloride shifted the NaCI sensitivity curve to the same degree in both groups and had virtually no effect on KCI thresholds. In addition, a more detailed analysis of chorda tympani nerve (CT) responses to NaCl, with and without benzarnil (Bz, an amiloride analog) treatment revealed that the tonic portion of the CT response of KO mice to NaCl(+) Bz was absent, but both KO and WT mice displayed some degree of a phasic response to NaCI with and without Bz. Because these transients constitute the entire CT response to NaCI(+) Bz in Trpvl KO mice, it is possible that these signals are sufficient to maintain normal NaCl detectabilty in the behavioral task used here, Additionally, there may be other amiloride-insensitive salt transduction mechanisms in taste receptor fields other than the anterior tongue that maintain normal salt detection performance in the KO mice.