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Regulation by spermine of native inward rectifier K+ channels in RBL-1 cells
L Bianchi1, M L Roy, M Taglialatela
1Rammelkamp Center for Education and Research, Case Western Reserve University School of Medicine, Cleveland, Ohio 44109-1998, USA.
The Journal of Biological Chemistry
|March 15, 1996
Summary
Polyamines influence potassium channel function. Inhibiting S-adenosylmethionine decarboxylase altered inward rectifier potassium currents and cell excitability, indicating spermine controls channel rectification.
Area of Science:
- Electrophysiology
- Cell Biology
- Pharmacology
Background:
- Polyamines modulate cloned inwardly rectifying potassium channels.
- Inwardly rectifying potassium channels (Kir) exhibit greater inward than outward current conduction.
- Understanding polyamine effects on native Kir channels is crucial.
Purpose of the Study:
- To investigate the impact of polyamine biosynthesis inhibitors on native inwardly rectifying potassium currents in rat basophil leukemia cells.
- To correlate changes in intracellular polyamine levels with electrophysiological properties and cell excitability.
Main Methods:
- Culturing rat basophil leukemia cells with polyamine biosynthesis inhibitors.
- Monitoring electrophysiological properties using patch-clamp techniques.
- Quantifying intracellular polyamine levels (putrescine, spermidine, spermine).
Main Results:
- Alpha-difluoromethylornithine (ornithine decarboxylase inhibitor) did not significantly alter electrophysiological properties.
- MDL73811 (S-adenosylmethionine decarboxylase inhibitor) increased outward currents and intracellular putrescine, while decreasing spermidine and spermine.
- Altered intracellular polyamine concentrations directly affected cell excitability.
Conclusions:
- The rectification properties of native inwardly rectifying potassium channels are significantly influenced by intracellular polyamine concentrations.
- Spermine appears to be a key regulator of the rectification characteristics of native inwardly rectifying potassium channels.