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Thrombin receptors activate potassium and chloride channels
R Sullivan1, D L Kunze, M H Kroll
1Research Service, Houston VA Medical Center, TX 77030, USA.
Blood
|January 15, 1996
Summary
Thrombin receptor activation in leukemia cells triggers complex membrane potential changes. This involves distinct calcium-independent chloride and calcium-activated potassium currents contributing to cell signaling.
Area of Science:
- Cellular Electrophysiology
- Ion Channel Function
- G-protein Coupled Receptor Signaling
Background:
- Thrombin receptor activation in platelets leads to calcium increases.
- DAMI human megakaryocytic leukemia cells express functional thrombin receptors.
- Understanding ion flux is crucial for cell signaling pathways.
Purpose of the Study:
- To investigate transmembrane ion currents activated by thrombin receptor signaling in DAMI cells.
- To characterize the membrane potential changes during thrombin receptor activation.
- To identify the specific ion conductances responsible for the observed electrophysiological responses.
Main Methods:
- Utilized DAMI human megakaryocytic leukemia cells.
- Stimulated cells with thrombin receptor-activating peptide.
- Monitored cytosolic Ca2+ ([Ca2+]i) levels.
- Measured individual cell membrane potentials using electrophysiological techniques.
Main Results:
- Thrombin receptor activation induced a rapid increase in [Ca2+]i.
- Observed complex, triphasic membrane potential changes: hyperpolarization, depolarization, and repolarization.
- Identified a Ca(2+)-independent, outwardly rectifying Cl- current.
- Discovered a Ba(2+)-sensitive, inwardly rectifying K+ current activated by increased [Ca2+]i.
Conclusions:
- The hyperpolarizing current is a composite of Cl- and K+ currents.
- These ion conductances likely regulate cell volume changes during thrombin receptor activation.
- The observed hyperpolarization may enhance Ca2+ influx by increasing the electromotive drive.