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Article
Identifying the Ca++ Signalling Sources Activating Chloride Currents in Xenopus Oocytes Using Ionomycin and Thapsigargin
Cellular Signalling (2000)
  • Carl L. Thurman, University of Northern Iowa
  • Jon S. Burns, University of Northern Iowa
  • Roger G O'Neil, University of Texas Medical School
Abstract
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 μM) and IM (0.1 to 10 μM) 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.
Disciplines
Publication Date
October, 2000
DOI
10.1016/S0898-6568(00)00106-6
Citation Information
Carl L. Thurman, Jon S. Burns and Roger G O'Neil. "Identifying the Ca++ Signalling Sources Activating Chloride Currents in Xenopus Oocytes Using Ionomycin and Thapsigargin" Cellular Signalling Vol. 12 Iss. 9-10 (2000) p. 629 - 635
Available at: http://works.bepress.com/carl_thurman/12/