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We use our sense of taste to determine if a potential food item should be consumed. Taste is activated when chemicals from potential nutrients activate the peripheral taste receptor cells in the mouth. Peripheral taste receptor cells depend on distinct calcium signals to generate appropriate cellular responses that relay taste information to the central nervous system. There are significant differences in the responses between taste cells, depending on what taste quality they detect. Some taste cells have conventional chemical synapses and rely on calcium influx through voltage-gated calcium channels. Other taste cells lack these synapses and depend on calcium release from stores to formulate an output signal. Regardless of the signaling pathway, taste cells all depend on calcium to form an appropriate output signal. This review will discuss the known differences between the taste signaling pathways and what is currently known about how these calcium signals are regulated. Emerging evidence suggests that diseases, such as obesity, can significantly alter taste-evoked calcium signals, which may lead to alterations in taste-dependent behaviors. Clearly, calcium signaling is a critical component of taste transduction and may be more complex than previously appreciated.

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