FIGURE 1.

Ca²⁺ signaling patterns evoked by CCK in pancreatic acinar cells extracted from wild type and CD38^−/− mice. Ca²⁺ oscillations were observed in wild type cells after 5 or 50 pm CCK stimulation (n = 40 and 18, respectively) in the presence (A) and absence (B) of Ca²⁺ in the extracellular solution (n = 27 and 22, respectively). C, cytosolic Ca²⁺ signals evoked by CCK at 5 pm in CD38^−/− cells (n = 37) in the presence of extracellular Ca²⁺. D, no Ca²⁺ responses were observed in cells extracted from CD38^−/− mice following stimulation with 5 or 50 pm CCK in Ca²⁺-free external solution, although the SERCA inhibitor, thapsigargin (1 μm; Tg) still evokes Ca²⁺ release (n = 87 and 86, respectively). E, whole cell configuration of the patch clamp technique recordings of the Ca²⁺-dependent Cl⁻ current in CD38^−/− acinar cells, which was used as an index of the cytosolic Ca²⁺ elevation. The Ca²⁺-sensitive current evoked by NAADP (50 nm) or by IP₃ at 15 μm or cADPR at 10 μm when present, respectively, in the intracellular pipette solution (n = 4, 3, and 3, respectively). The messenger-evoked Ca²⁺ spikes are similar to those observed in pancreatic acinar cells derived from wild type mice (7, 27).