Calcium oscillations in pancreatic acinar cells can take radically different forms depending on the type of agonist used to stimulate them. For instance, CCK gives, typically, low frequency baseline spikes, while ACh gives faster oscillations on a raised baseline. I shall present a model that describes both oscillation types, discuss predictions from the model, and present new experimental data that confirms the model predictions. Our data show that CCK causes much greater phosphorylation of the IP3 receptor, modulates the calcium influx pathway, and decreases the rate of Ca-ATPase activity; we show that these differences are sufficient to explain the different kinds of oscillations.
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