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. Author manuscript; available in PMC: 2016 Sep 1.
Published in final edited form as: Biochim Biophys Acta. 2014 Nov 16;1853(9):2025–2032. doi: 10.1016/j.bbamcr.2014.11.013

Figure 2. Sodium/calcium exchangers significantly regulate evoked calcium influx signals but do not contribute to the reduction of the evoked calcium release from internal stores.

Figure 2

A, Replacing external sodium with lithium (light gray column) caused a reversible increase in cytosolic calcium levels while a 10s application of 50mM KCl (arrow) depolarized the taste cells and opened VGCCs. The calcium influx through the VGCCs generated a large increase in cytosolic calcium that slowly returned to baseline levels. B, The integrated area under the 50mM KCl + lithium elevation was significantly larger than the combination of the integrated areas for the calcium elevations that occurred when 50mM KCl and lithium were applied individually (***p<0.001). Adding the area of the 50mM KCl-evoked calcium response (light gray column) to the integrated area of the calcium response when NCXs were inhibited (dark gray column) was only 79% of the integrated area of the calcium response that was generated when VGCCs were open while NCXs were inhibited (striped column). C, Replacing external sodium with lithium (Li) caused a reversible increase in cytosolic calcium levels while a 30s application of the bitter compound, 10mM denatonium benzoate (D) caused calcium release from internal stores. When bitter receptors were activated while NCXs were inhibited, the cytosolic calcium response increased. D, The integrated area under the lithium + denatonium response (Li + Den, striped column) was approximately equal to the combination of the integrated areas for the calcium signals that occurred when denatonium (light gray column) and lithium (dark gray column) were applied individually. Reprinted from Szenbenyi et al., (2010).