Purpose: In non-excitable cells, which include parotid and pancreatic acinar cells, Ca2+ entry is triggered via a mechanism known as capacitative Ca2+ entry, or store-operated C2+ entry. This process is initiated by the perception of the filling state of endoplasmic reticulum (ER) and the depletion of internal Ca2+ stores, which acts as an important factor triggering Ca2+ entry. However, both the mechanism of store-mediated Ca2+ entry and the molecular identity of store-operated Ca2+ channel (SOCC) remain uncertain. Materials and Methods: In the present study we investigated the Ca2+ entry initiation site evoked by depletion of ER to identify die localization of SOCC in mouse parotid and pancreatic acinar cells with microfluorometeric imaging system. Results: Treatment with thapsigargin (Tg), an inhibitor of sarco/ endoplasmic reticulum Ca2+-ATPase, in an extracellular Ca2+ free state, and subsequent exposure to a high external calcium state evoked Ca2+ entry, while treatment with lanthanum, a non-specific blocker of plasma Ca2+ channel, completely blocked Tg-induced Ca2+ entry. Mcrofluorometric imaging showed that Tg-induced Ca2+ entry started at a basal membrane, not a apical membrane. Conclusion: These results suggest that Ca2+ entry by depletion of the ER initiates at the basal pole in polarized exocrine cells and may help to characterize the nature of SOCC.
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