Chorda tympani nerve transection, but not amiloride, increases the KCl taste detection threshold in rats.

Geran, Laura C.; Guagliardo, Nick A.; Spector, Alan C.

doi:10.1037/0735-7044.113.1.185

Cited by 18 publications

(30 citation statements)

References 54 publications

(84 reference statements)

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“…In rats, the detection threshold for NaCl with 100 M amiloride is similar to the detection threshold for KCl (14,15). On the basis of these studies, we would have expected the KCl detection thresholds in B6 and Trpv1 KO mice to be similar with those seen for NaCl when it is adulterated with amiloride.…”

Section: Discussionmentioning

confidence: 69%

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

Treesukosol

Lyall

Heck

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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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 1 (TRPV1) that serves as a nonspecific cation channel. To provide a functional context for these findings, we trained Trpv1 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 NaCl sensitivity curve to the same degree in both groups and had virtually no effect on KCl thresholds. In addition, a more detailed analysis of chorda tympani nerve (CT) responses to NaCl, with and without benzamil (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 NaCl with and without Bz. Because these transients constitute the entire CT response to NaCl + Bz in Trpv1 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.

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Section: Discussionmentioning

confidence: 69%

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

Treesukosol

Lyall

Heck

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…This suggests that recognition and discrimination of these salts depends on amiloride-insensitive, saltresponsive units in these nerves. As noted previously, normal KCl detectability is also compromised by CT transection but not significantly affected by amiloride treatment, suggesting that AI units of the facial nerve are required for this task (Geran et al, 1999). Although the AI pathway does not appear to be necessary for rats to increase sodium intake when depleted of sodium, this route of transduction could be important for the satiation of other mineral appetites like that induced by calcium deprivation.…”

Section: Discussionmentioning

confidence: 74%

Anion Size Does Not Compromise Sodium Recognition by Rats After Acute Sodium Depletion.

Geran¹,

Spector²

2004

Behavioral Neuroscience

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Amiloride-insensitive sodium taste transduction is severely limited by large anions (i.e., gluconate). We found that in a brief-access taste test, sodium-depleted rats exhibited similar levels of increased licking to several sodium salts regardless of anion but did not increase licking to nonsodium salts compared with water. The enhanced licking of sodium salts was abolished in the presence of amiloride. These results suggest that the amiloride-sensitive taste transduction pathway is not only necessary but that it is also sufficient for sodium identification in rats. Sodium-depleted rats tested with amiloride initiated significantly more trials than nondepleted rats; hence, appetitive behavior was mildly potentiated by depletion, even in the absence of a sodium taste cue. Overall, these findings provide compelling support for the primacy of the amiloride-sensitive taste transduction mechanism and its associated neural pathway in the recognition of the sodium cation.

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“…However, there is one published study in which detection thresholds to sucrose and monosodium glutamate (MSG) were measured in T1R3 KO and WT mice through the use of a shock avoidance procedure. Generally, manipulations of the gustatory system that have major effects on neural responses to taste stimuli are reflected in shifts in sensory thresholds in animal models [e.g.,7, 22, 30, 97, 102, 104, 112], but T1R3 KO mice had normal detection thresholds for both sucrose and MSG compared with WT mice [17]. Considering the evidence in the literature supporting the role of T1R2 and T1R3 in mediating sucrose taste, it would be expected that T1R3 KO mice would at least have elevated, as opposed to normal, sucrose detection thresholds.…”

Section: Taste Functionmentioning

confidence: 99%

The functional role of the T1R family of receptors in sweet taste and feeding

Treesukosol

Smith

Spector

2011

Physiology & Behavior

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The discovery of the T1R family of Class C G protein-coupled receptors in the peripheral gustatory system a decade ago has been a tremendous advance for taste research, and its conceptual reach has extended to other organ systems. There are three proteins in the family, T1R1, T1R2, and T1R3, encoded by their respective genes, Tas1r1, Tas1r2, and Tas1r3. T1R2 combines with T1R3 to form a heterodimer that binds with sugars and other sweeteners. T1R3 also combines with T1R1 to form a heterodimer that binds with L-amino acids. These proteins are expressed not only in taste bud cells, but one or more of these T1Rs have also been identified in the nasal epithelium, gut, pancreas, liver, kidney, testes and brain in various mammalian species. Here we review current perspectives regarding the functional role of these receptors, concentrating on sweet taste and feeding. We also discuss behavioral findings suggesting that a glucose polymer mixture, Polycose, which rodents avidly prefer, appears to activate a receptor that does not depend on the combined expression of T1R2 and T1R3. In addition, although the T1Rs have been implicated as playing a role in glucose sensing, T1R2 knock-out (KO) and T1R3 KO mice display normal chow and fluid intake as well as normal body weight compared with same-sex littermate wild type (WT) controls. Moreover, regardless of whether they are fasted or not, these KO mice do not differ from their WT counterparts in their Polycose intake across a broad range of concentrations in 30-min intake tests. The functional implications of these results and those in the literature are considered.

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Chorda tympani nerve transection, but not amiloride, increases the KCl taste detection threshold in rats.

Cited by 18 publications

References 54 publications

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

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

Anion Size Does Not Compromise Sodium Recognition by Rats After Acute Sodium Depletion.

The functional role of the T1R family of receptors in sweet taste and feeding

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