Cell Signal 2000 Oct 01;129-10:629-35. doi: 10.1016/s0898-6568(00)00106-6.

Identifying the Ca(++) signalling sources activating chloride currents in Xenopus oocytes using ionomycin and thapsigargin.

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The calcium ionophore, ionomycin (IM), and the sarcoplasmic/endoplasmic reticulum (SER) calcium pump inhibitor, thapsigargin (TG), were used to study the roles of Ca(++) from different sources in regulating Ca(++)-dependent Cl(-) currents in Xenopus oocytes. The Ca(++)-dependent Cl(-) currents, Ic, were measured in voltage-clamped oocytes (Vc = -60 mV). In the presence of extracellular Ca(++), both TG (0.1 to 10 microM) and IM (0.1 to 10 microM) induce release of Ca(++) from SER and activated capacitative Ca(++) entry (CCE) across the plasma membrane leading to activation of both "fast" and "slow" Cl(-) currents. The fast Ic was produced by Ca(++) release from SER while Ca(++) entry across the plasma membrane activated the slow Ic. Intracellular application of the calcium buffer, BAPTA, blocked activation of the slow Ic due to Ca(++) entry via CCE pathways, but not via IM-mediated movement across the plasma membrane. It is concluded that predominantly Ca(++) release from stores regulates a fast Ic while Ca(++) entry through CCE pathways regulates a slow Ic. Further, the CCE and slow Ic pathways must be located in spatially separated compartments since BAPTA can effectively abolish the effects of Ca(++) entry via the CCE pathway, but not by the IM-mediated entry pathway.

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