1. Quinine inhibits Ca2+ -independent K+ channels whereas tetraethylammonium inhibits Ca2+ -activated K+ channels in insulin-secreting cells
- Author
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M. J. Dunne, I. Findlay, Ole H. Petersen, Susanne Ullrich, and Claes B. Wollheim
- Subjects
medicine.medical_specialty ,RINm5F cell ,K+ channel ,Potassium ,Biophysics ,chemistry.chemical_element ,Calcium ,Biochemistry ,Ion Channels ,Cell Line ,chemistry.chemical_compound ,Structural Biology ,Internal medicine ,Genetics ,medicine ,Animals ,Patch clamp ,Molecular Biology ,Membrane potential ,Tetraethylammonium ,Quinine ,Chemistry ,Inward-rectifier potassium ion channel ,Cell Membrane ,Electric Conductivity ,Cell Biology ,Tetraethylammonium Compounds ,Hyperpolarization (biology) ,Adenoma, Islet Cell ,Pancreatic Neoplasms ,Membrane ,Endocrinology ,Insulinoma - Abstract
The effects of quinine and tetraethylammonium (TEA) on single-channel K + currents recorded from excised membrane patches of the insulin-secreting cell line RINm5F were investigated. When 100 μM quinine was applied to the external membrane surface K + current flow through inward rectifier channels was abolished, while a separate voltage-activated high-conductance K + channel was not significantly affected. On the other hand, 2 mM TEA abolished current flow through voltage-activated high-conductance K + channels without influencing the inward rectifier K + channel. Quinine is therefore not a specific inhibitor of Ca 2+ -activated K + channels, but instead a good blocker of the Ca 2+ -independent K + inward rectifier channel whereas TEA specifically inhibits the high-conductance voltage-activated K + channel which is also Ca 2+ -activated.
- Published
- 1985
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