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>Hypothesis of Receptor-Dependent and Receptor-Independent Mechanisms for Bitter and Sweet Taste Transduction: Implications for Slow Taste Onset and Lingering Aftertaste
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Hypothesis of Receptor-Dependent and Receptor-Independent Mechanisms for Bitter and Sweet Taste Transduction: Implications for Slow Taste Onset and Lingering Aftertaste
Signal messengers such as cAMP, IP_3 and cGMP in taste cells following bitter and sweet taste stimulation can be monitored in real time, in the subsecond range. However, many amphipathic sweeteners and bitter tastants are slow in taste onset and linger, and the molecular basis for these temporal properties is ill-defined. The bitter tastants quinine and cyclo(Leu-Trp), and the non-sugar sweetener saccharin, permeate rapidly through liposomes and taste cells. Furthermore, amphipathic bitter tastants appear to interact with and/or permeate phospholipid-based bitter taste inhibitors. Thus, bitter taste is masked by preventing access of these tastants to taste cells. Such tastants can stimulate responses in cells that are not related to taste cells, and are therefore unlikely to contain taste receptors. It is hypothesized that due to their rapid permeation into taste cells, these tastants may activate the downstream transduction components directly, in addition to their action on G-protein-coupled receptors. The delayed temporal properties produced by many bitter tastants and non-sugar sweeteners may be related to this phenomenon.
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