Faculty Publications

Identifying The Ca++ Signalling Sources Activating Chloride Currents In Xenopus Oocytes Using Ionomycin And Thapsigargin

Document Type

Article

Journal/Book/Conference Title

Cellular Signalling

Volume

12

Issue

9-10

First Page

629

Last Page

635

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.

Department

Department of Biology

Original Publication Date

11-29-2000

DOI of published version

10.1016/S0898-6568(00)00106-6

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