Figure 5.

Intracellular Ca²⁺ release in Presynaptic (Type III) cells is via a PLC-mediated pathway. A, Presynaptic (Type III) cells were initially stimulated with KCl (50 mm) to verify its identity (data not shown). Bath application of CGRP (0.1 μm) elicits Ca²⁺ mobilization in the taste cell (↓, CGRP). Treating Presynaptic (Type III) cells with thapsigargin (1 μm), a SER Ca-ATPase inhibitor (present throughout the shaded area), irreversibly reduced Ca²⁺ responses evoked by CGRP, consistent with Ca²⁺ store release mechanisms for these stimuli. B, Summary of CGRP-elicited Ca²⁺ responses before, during, and after the presence of thapsigargin. Points indicate normalized peak taste cell responses. Blue symbols represent mean ± 95% CI. ***p < 0.001 (paired Student's t test). N = 4. ns, Not significant. C, CGRP-elicited Ca²⁺ mobilization in an isolated Presynaptic (Type III) cell, identified by its responses to KCl, but not taste, was blocked when U73122 (10 μm) (present throughout the shaded area) was present in the bathing solution. Consistent with the blockage of PLC-mediated cascade, these findings indicated that CGRP-elicited responses in Presynaptic (Type III) cells were due to Ca²⁺ release from intracellular stores. D, Summary of experiments plotted as in C. *p < 0.05, ***p < 0.001 (paired Student's t test). N = 4.