Understanding how the taste system functions is an important first step in any attempt to modulate taste perception. Ultimately, making products more appetitive for consumption depends on affecting the cellular processes that are required for normal taste transduction. Taste begins in the oral cavity when chemicals from potential food items activate peripheral taste receptor cells. These taste cells are the critical first step in taste and if they are dysfunctional, subsequent taste perception will be affected. Taste cells in the oral cavity are also easily accessible which makes them an attractive target for manipulation. To effectively modulate taste cell activity, it’s imperative that there is a good understanding of how these cells function in their normal state. Taste cells use multiple signaling pathways to transduce taste stimuli into output signals that are sent to the brain. Salty and sour stimuli bind ion channels to cause cell depolarization, while bitter, sweet and umami stimuli activate a G-protein coupled receptor (GPCR) signaling pathway. It is currently thought that while GPCRs for bitter, sweet and umami are selective for these different stimuli and are expressed in different cell populations, they all use the same downstream signaling pathway. This downstream pathway includes activation of phospholipase C β2 (PLCβ2) which produces IP3 to activate IP3 Receptors and cause calcium release from internal stores. This calcium release activates Transient Receptor Potential Melastatin 5 (TRPM5), a sodium selective TRP channel which depolarizes the cells and triggers neurotransmitter release. Several studies have cast doubt on this model but no alternatives have been proposed. Recent work from my lab indicates that this current model for the transduction of bitter, sweet and umami stimuli is an oversimplification and that additional signaling proteins also have critical roles in the transduction of taste stimuli.

New insights into peripheral taste signaling pathways

256th National Meeting (2018)

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