Calcium signaling in mouse taste cells
Rebello, Michelle R. L.
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Taste cells convert the chemical stimulus of the food we eat into an electrical signal that can be recognized by afferent nerve fibers. They do so using distinct cytosolic calcium signals that are directly related to synaptic output and are therefore under tight regulation. These calcium signals can originate either via calcium release from intracellular stores or from calcium influx through voltage-gated channels. They are then terminated by various calcium clearance mechanisms. This is the first study to show that ryanodine receptors type 1 are expressed in mouse taste cells and contribute to taste stimulus evoked-calcium release from stores in a sub-population of taste cells. I have also shown that the calcium influx signal is predominantly due to the high voltage activated L-type and the low voltage activated T-type calcium channels. In some taste cells, L-type channels functionally associate with ryanodine receptors and enhance the depolarization-induced calcium influx signal. One of the means of terminating these calcium signals is by the binding of free cytosolic calcium to calcium binding proteins. I have characterized the distribution of calcium binding proteins such as calretinin, calbindin, parvalbumin, CaBP and neurocalcin in a sub-population of taste cells. These calcium-binding proteins are differentially expressed within taste cells, which may be a reflection of their functional properties. Taste cells have therefore evolved complex and varied mechanisms to effectively control cytosolic calcium signals.