The initial objective of this study was to determine if activation of the sweet taste receptor TAS1R2/TAS1R3 is necessary for perception of sweet thermal taste. Our approach was to inhibit the receptor with the inverse agonist lactisole using a temperature-controlled flow gustometer. Because all prior studies of thermal taste used metal thermodes to heat the tongue tip, we first investigated whether it could be generated in heated water. Experiment 1 showed that sweetness could be evoked when deionized water was heated from 20° to 35°C, and testing with static temperatures between 20° and 35°C demonstrated the importance of heating from a cool temperature. As in previous studies, thermal sweetness was reported by only a subset of participants, and replicate measurements found variability in reports of sweetness across trials and between sessions. Experiment 2 then showed that exposure to 8mM lactisole blocked perception of sweet thermal taste. Confirmation of the involvement of TAS1R2/TAS1R3 led to an investigation of possible sensory and cognitive interactions between thermal and chemical sweetness. Using sucrose as a sweet stimulus and quinine as a non-sweet control, we found that dynamic heating capable of producing thermal sweetness did not increase the sweetness of sucrose compared to static heating at 35°C. However, sweet thermal taste was disrupted if trials containing sucrose (but not quinine) were interspersed among heating-only trials. These findings provide new information relevant to understanding the perceptual processes and receptor mechanisms of sweet thermal taste, as well as the heat sensitivity of sweet taste in general.

Initial sensitivity would not be reduced and adaptation would tend to be reversed as the solution warms in the mouth. However, none of these findings ruled out the possibility that colder temperatures affect sweet taste independently of adaptation. In particular, lower temperatures might reduce the excitability of the calcium-dependent channel TRPM5, which is the final step in the T1R2–T1R3 sweet taste receptor transduction cascade that leads to receptor depolarization ( Liman 2007 ). Talavera et al. (2005) reported that when expressed in HEK-293 cells, activation of TRPM5 by intracellular Ca 2+ is strongly modulated by temperatures below 30 °C and proposed that TRPM5 is responsible for the temperature sensitivity of sweet taste. Because lower solution temperatures are likely to be necessary to produce equivalent cooling of TRPM5 in vivo, we hypothesized that temperatures below 21 °C might reduce human sweet taste sensitivity consistent with the effect of cold on sweet-specialist neurons in the geniculate ganglion of rats ( Breza et al. 2006 ) and medulla of mice ( Wilson and Lemon 2014 ). We investigated this hypothesis and sought to replicate our earlier findings on sweet taste adaptation in 3 experiments. The first experiment confirmed the effect on sucrose adaptation at 21 °C and below, and further showed that at 5 and 10 °C, the initial sweetness of sucrose, glucose, and fructose was also reduced. The second experiment used the same procedure to compare the effects of temperature on the sweetness of 3 artificial sweeteners, and a final experiment employed a temperature and flow-controlled gustometer to rule out the possibility that the effects of temperature on sweetness in the first 2 experiments were unique to dipping the tongue into a still taste solution. Materials and methods Experiment 1: the effects of temperature on sweetness and adaptation for sugars Subjects A total of 27 adults (18 females and 9 males) between 18 and 45 years of age served as subject