Salivary proteins alter taste-guided behaviors and taste nerve signaling in rat.

Taste stimuli are normally dissolved in saliva prior to interacting with their respective receptor targets. There are hundreds of proteins in saliva, and it has been hypothesized that these proteins could interact with either taste stimuli or taste receptors to alter taste signaling and diet acceptance. However, the impact of these proteins on feeding has been relatively unexplored using rodent models.

Contribution of the TRPV1 channel to salt taste quality in mice as assessed by conditioned taste aversion generalization and chorda tympani nerve responses.

In rodents, at least two transduction mechanisms are involved in salt taste: 1) the sodium-selective epithelial sodium channel, blocked by topical amiloride administration, and 2) one or more amiloride-insensitive cation-nonselective pathways. Whereas electrophysiological evidence from the chorda tympani nerve (CT) has implicated the transient receptor potential vanilloid-1 (TRPV1) channel as a major component of amiloride-insensitive salt taste transduction, behavioral results have provided only equivocal support. Using a brief-access taste test, we examined generalization profiles of water-deprived C57BL/6J (WT) and TRPV1 knockout (KO) mice conditioned (via LiCl injection) to avoid 100 μM amiloride-prepared 0.

Leptin increases temperature-dependent chorda tympani nerve responses to sucrose in mice.

Leptin receptors are present in taste buds and previous research indicates that leptin administration modified electrophysiological and behavioral responses to sweet taste. It is now known that sweet taste is temperature dependent. We examined the influence of (1) stimulus temperature on chorda tympani (CT) nerve responses to sucrose, saccharin and NH(4)Cl; and (2) leptin administration on CT nerve responses to sucrose, saccharin and other basic taste stimuli at 35°C that maximized sweet-taste sensitivity in C57BL/6 mice.