Sodium–calcium exchangers contribute to the regulation of cytosolic calcium levels in mouse taste cells

Authors


Corresponding author K. Medler: Department of Biological Sciences, University at Buffalo, The State University of New York, Buffalo, NY 14260, USA. Email: kmedler@buffalo.edu

Abstract

Taste cells use multiple signalling mechanisms to generate unique calcium responses to distinct taste stimuli. Some taste stimuli activate G-protein coupled receptors (GPCRs) that cause calcium release from intracellular stores while other stimuli depolarize taste cells to cause calcium influx through voltage-gated calcium channels (VGCCs). We recently demonstrated that a constitutive calcium influx exists in taste cells that is regulated by mitochondrial calcium transport and that the magnitude of this calcium influx correlates with the signalling mechanisms used by the taste cells. In this study, we used calcium imaging to determine that sodium–calcium exchangers (NCXs) also routinely contribute to the regulation of basal cytosolic calcium and that their relative role correlates with the signalling mechanisms used by the taste cells. RT-PCR analysis revealed that multiple NCXs and sodium–calcium–potassium exchangers (NCKXs) are expressed in taste cells. Thus, a dynamic relationship exists between calcium leak channels and calcium regulatory mechanisms in taste cells that functions to keep cytosolic calcium levels in the appropriate range for cell function.

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