Mitochondrial calcium buffering contributes to the maintenance of Basal calcium levels in mouse taste cells.
Taste stimuli are detected by taste receptor cells present in the oral cavity using diverse signaling pathways. Some taste stimuli are detected by G protein-coupled receptors (GPCRs) that cause calcium release from intracellular stores, whereas other stimuli depolarize taste cells to cause calcium influx through voltage-gated calcium channels (VGCCs). Although taste cells use two distinct mechanisms to transmit taste signals, increases in cytosolic calcium are critical for normal responses in both pathways. This creates a need to tightly control intracellular calcium levels in all transducing taste cells. To date, however, the mechanisms used by taste cells to regulate cytosolic calcium levels have not been identified. Studies in other cell types have shown that mitochondria can be important calcium buffers, even during small changes in calcium loads. In this study, we used calcium imaging to characterize the role of mitochondria in buffering calcium levels in taste cells. We discovered that mitochondria make important contributions to the maintenance of resting calcium levels in taste cells by routinely buffering a constitutive calcium influx across the plasma membrane. This is unusual because in other cell types, mitochondrial calcium buffering primarily affects large evoked calcium responses. We also found that the amount of calcium that is buffered by mitochondria varies with the signaling pathways used by the taste cells. A transient receptor potential (TRP) channel, likely TRPV1 or a taste variant of TRPV1, contributes to the constitutive calcium influx.
Hacker
Kyle
K
Department of Biological Sciences, University at Buffalo, The State University of New York, Buffalo, NY 14260, USA.
Medler
Kathryn F
KF
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000502:physiology; D000818:Animals; D002021:Buffers; D002118:Calcium / Q000378:metabolism* / Q000502:physiology*; D020013:Calcium Signaling / Q000502:physiology*; D002259:Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone / Q000494:pharmacology; D002462:Cell Membrane / Q000201:enzymology / Q000502:physiology; D003600:Cytosol / Q000378:metabolism / Q000502:physiology; D004721:Endoplasmic Reticulum / Q000201:enzymology / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D051379:Mice; D008810:Mice, Inbred C57BL; D008928:Mitochondria / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology; D050916:TRPV Cation Channels / Q000037:antagonists & inhibitors; D013650:Taste Buds / Q000166:cytology* / Q000378:metabolism / Q000502:physiology*; D019284:Thapsigargin / Q000494:pharmacology
D002021:Buffers; D004791:Enzyme Inhibitors; D050916:TRPV Cation Channels; C493921:TRPV1 protein, mouse; D002259:Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone; D019284:Thapsigargin; D000255:Adenosine Triphosphate; D000251:Adenosine Triphosphatases; D002118:Calcium