Sodium/calcium exchangers selectively regulate calcium signaling in mouse taste receptor cells.
Sodium/calcium exchangers selectively regulate calcium signaling in mouse taste receptor cells.
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DOI：
10.1152/jn.00118.2010
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发表时间：
2010-05
影响因子：
2.5
通讯作者：
Steven A. Szebenyi;Agnieszka I. Laskowski;K. Medler
中科院分区：
文献类型：
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作者：
Steven A. Szebenyi;Agnieszka I. Laskowski;K. Medler
味觉细胞使用多种信号传导机制来对离散的味觉刺激产生适当的细胞反应。一些味觉刺激物激活G蛋白偶联受体（GPCR），其引起钙从细胞内储存释放，而其他刺激物使味觉细胞变性以引起钙通过电压门控钙通道（VGCC）流入。虽然已经在味觉细胞中描述了启动钙信号的信号传导机制，但是尚未鉴定出有助于终止这些信号的钙清除机制（CCM）。在这项研究中，我们使用钙成像来确定钠钙交换剂（NCXs）在终止诱发钙反应中的作用。我们发现，NCXs调节依赖于质膜钙内流的钙信号，但对依赖于内部储存的钙释放的钙信号没有显着贡献。我们的数据表明，这种选择性调节钙信号的NCXs主要是由于它们在细胞中的位置，而不是在细胞溶质钙负荷的差异。这是第一份报告，以确定的生理作用的任何CCM利用味觉细胞调节其诱发的钙反应。
Taste cells use multiple signaling mechanisms to generate appropriate cellular responses to discrete 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). While the signaling mechanisms that initiate calcium signals have been described in taste cells, the calcium clearance mechanisms (CCMs) that contribute to the termination of these signals have not been identified. In this study, we used calcium imaging to define the role of sodium-calcium exchangers (NCXs) in the termination of evoked calcium responses. We found that NCXs regulate the calcium signals that rely on calcium influx at the plasma membrane but do not significantly contribute to the calcium signals that depend on calcium release from internal stores. Our data indicate that this selective regulation of calcium signals by NCXs is due primarily to their location in the cell rather than to the differences in cytosolic calcium loads. This is the first report to define the physiological role for any of the CCMs utilized by taste cells to regulate their evoked calcium responses.