Sodium aspartate as a specific enhancer of salty taste perception-sodium aspartate is a possible candidate to decrease excessive intake of dietary salt.

The excessive intake of dietary salt is a global issue in health. Attempts have been made to address this issue, including the development of salt substitutes. Yet, none of these substances are currently in wide use, because of their weak saltiness. The purpose of this study was to assess the effects of sodium aspartate (Asp-Na) on salty taste perception using the bullfrog glossopharyngeal nerve response and human sensory tests. When added to the mixture of NaCl and KCl, Asp-Na significantly enhanced the glossopharyngeal nerve response to the mixture by 1.6-fold compared to control. Asp-Na did not enhance the response to NaCl, nor did Asp-Na enhance the response to sour, bitter, or umami stimuli. The optimal concentration for Asp-Na to enhance the salt mixture was 1.7mM. The largest enhancement was induced when NaCl and KCl were mixed at equimolar concentrations. Asp-Na significantly suppressed the glossopharyngeal nerve response to quinine hydrochloride, which suggests that bitterness of KCl is suppressed by Asp-Na. The salty taste enhancing effect of Asp-Na was also confirmed with human sensory tests. The present results suggested that the mixture of NaCl and KCl containing Asp-Na can be used as a salt substitute. In addition to demonstrating that Asp-Na enhanced salt taste responses in an experimental animal and human, our findings provide clues to identify the elusive salty taste receptors.

Characterization of electro-olfactogram oscillations and their computational reconstruction.

Electro-olfactogram (EOG) oscillations induced by odorant stimulation have been often reported in various vertebrates from fishes to mammals. However, the mechanism of generation of EOG oscillations remains unclear. In the present study, we first characterized the properties of EOG oscillations induced by amino acid odorants in the rainbow trout and then performed a computer simulation based on the main assumption that olfactory receptor neurons (ORNs) have intrinsic oscillatory properties due to two types of voltage-gated ion channels, which have not yet been reported in vertebrate ORNs. EOG oscillations appeared mostly on the peak and decay phases of negative EOG responses, when odorant stimuli at high intensity flowed regularly anterior to posterior olfactory lamellae in the olfactory organ. The appearance of EOG oscillations was dependent on the odorant intensity but not on the flow rate. The maximum amplitude and the maximum power frequency of EOG oscillations were 3.51 +/- 3.35 mV (mean +/- SD, n = 232, range 0.12-16.79 mV) and 10.59 +/- 5.05 Hz (mean +/- SD, n = 232, range 3.51-40.03 Hz), respectively. The simulation represented sufficiently well the characteristics of EOG oscillations; occurrence at high odorant concentration, odorant concentration-dependent amplitude and the maximum power frequency range actually observed. Our results suggest that EOG oscillations are due to the intrinsic oscillatory properties of individual ORNs, which have two novel types of voltage-gated ion channels (resonant and amplifying channels). The simulation program for Macintosh ('oscillation 3.2.4' for MacOS 8.6 or later) is available on the world wide web (http://bio2.sci.hokudai.ac.jp/bio/chinou1/noriyo_home.html).