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magnesium regulates the Kcnql/Kcnel channel function via the C-terminal of Kcnel subunit

Magnesium regulates the Kcnql/Kcnel channel function via the...

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中国神经科学学会第四次会员代表大会暨第七届全国学术会议

作者： Zhi-Jun SHEN Ion Channel Disease Lab,Department of Physiology and Pharmacology,Key Lab of Development and Disease Related Genes,School of Basic Medical Science,Southeast University School of Medicine,Nanjing 210009,China

＜正＞The voltage-dependent potassium channel Kv7.1 is a tetramer composed of Kcnq1 a and Kcnel b subunits.It has been found functionally expressed in heart,inner ear,kidney and colons and mediating depolarization in the cardiac myocytes and potassium secretion into endolymph in the inner ear epithelial cells and assisting chloride homeostasis in epithelium of kidney and colons under physiological condition.Regulatory mechanisms of the channel function via adrenergic and purinergic receptors are well documented.Inherited mutations found in both kcnql and kcnel gene have been directly linked to clinical phenotypes of dominant form of Long QT syndrome with hearing loss（Jervell-Lange-Neilson Syndrome） and recessive form of Long QT syndrome without hearing loss（Romano-Word Syndrome）,which could be duplicated in experimental animals with gene engineering of knock-out and/or transgenic techniques.Here,we report that the intracellular magnesium is critical to the physiological function of the Kcnq 1/Kcne 1 channel.Using native inner ear epithelial cells,we recorded a voltage-dependent slowly activating current from the apical membrane via a macropatch on-cell configuration.The current was potassium selective and sensitive to the specific blocker of the Kcnq1/Kcne1 channel,chromano1 293B.Under excised or conventional whole cell configurations,we found that intracellular magnesium at assumed physiological levels was inhibitory to the function of the channel.The current was gradually running down upon excising or establishing the whole cell,and totally disappeared within 2-3 min.Adding ATP or Phosphatase inhibitor did not prevent the run-down.Elimination of magnesium in the background of physiological calcium levels could not only well keep the channel alive,but also significantly boosted the current 5-10 folds of its previous levels.Furthermore,the magnesium-free condition changed the voltage-dependency of the channel.It appeared that the channel carried two components under the magnesium-free condition;an instantaneous and

关键词： Kcnql/Kcnel channel intracellular magnesium C-terminal

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