POTASSIUM AND SODIUM-CHANNELS IN HUMAN-MALIGNANT GLIOMA-CELLS

POTASSIUM AND SODIUM-CHANNELS IN HUMAN-MALIGNANT GLIOMA-CELLS
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DOI:
10.1016/0006-8993(89)90191-1
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发表时间:
1989-02-20
期刊:
影响因子:
2.9
通讯作者:
COLLINS, VP
COLLINS, VP
中科院分区:
医学3区
文献类型:
--
作者:
BRISMAR, T;COLLINS, VP

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将来自5种不同细胞系的人恶性胶质瘤细胞进行电压钳位,并检查去极化激活离子通道的存在。在>40 mV的膜电位下诱发外向K电流,其具有两个主要成分,一个被外部施加的四乙基铵(TEA,10 mM)延迟并阻断,另一个是瞬时的并且对外部溶液中的TEA不敏感。两个K电流分量的比例在细胞系之间变化。在0-4 mM范围内的[Ca 2 +]o的增加降低了泄漏电导,并将瞬时外向K电流的激活向更正的电位转移。Mg ~(2+)、Zn ~(2+)和Co ~(2+)具有定性相似的作用。在膜两侧用150-160 mM K+溶液进行的斑贴记录表明,延迟的外向K-电流通过大电导(250-300 pS)通道进行。游离[Ca 2 +]i从0到2x的变化10-8 M增加了大电导K通道的激活。在来自一个细胞系(Tp-378 MG)的细胞中鉴定了小Na电流。Na电导在25%的细胞中在0.5至7.5 nS范围内,并且在75%中小于0.5 nS。Na-通道在比哺乳动物外周神经多30-40 mV的正电位下被激活和失活。河豚毒素(100 nM)几乎完全阻断gNa。
Human malignant glioma cells from 5 different cell lines were voltage clamped and examined for the presence of depolarization-activated ion channels. Outward K-currents were elicited at membrane potentials >40 mV, which had two main components, one which was delayed and blocked by externally applied tetraethylammonium (TEA, 10 mM), and another which was instantaneous and insensitive to TEA in the outside solution. The proportion of the two K-current components varied between cell lines. An increase in [Ca2+]o in the range 0-4 mM, decreased the leak conductance and shifted the activation of the instantaneous outward K-current towards more positive potentials. Mg2+, Zn2+ and Co2+ had qualitatively similar effects. Patch recordings with 150-160 mM K+ -solution on both sides of the membrane revealed that the delayed outward K-current was carried through large conductance (250-300 pS) channels. Changes in free [Ca2+]i from 0 to 2 .times. 10-8 M increased the activation of the large conductance K-channel. Small Na-currents were identified in cells from one cell line (Tp-378MG). The Na-conductance ranged from 0.5 to 7.5 nS in 25% of the cells, and was less than 0.5 nS in 75%. The Na-channels were activated and inactivated at 30-40 mV more positive potentials than in the mammalian peripheral nerve. Tetrodotoxin (100 nM) blocked gNa almost completely.