大鼠脑钾离子通道RCK家族一个新成员的电生理特性

Electrophysiological characterization of a new member of the RCK family of rat brain K+ channels.

作者信息

Kirsch G E, Drewe J A, Verma S, Brown A M, Joho R H

机构信息

Department of Anesthesiology, Baylor College of Medicine, Houston, TX 77030.

出版信息

FEBS Lett. 1991 Jan 14;278(1):55-60. doi: 10.1016/0014-5793(91)80082-e.

DOI:10.1016/0014-5793(91)80082-e

PMID:1993474

Abstract

A novel member of the RCK family of rat brain K+ channels, called RCK2, has been sequenced and expressed in Xenopus oocytes. The K+ currents were voltage-dependent, activated within 20 ms (at 0 mV), did not inactivate in 5 s, and had a single channel conductance in frog Ringers of 8.2 pS. Compared to other members of the RCK family the pharmacological profile of RCK2 was unique in that the channel was resistant to block (IC50 = 3.3 microM) by charybdotoxin [(1988) Proc. Natl. Acad. Sci. USA 85, 3329-3333] but relatively sensitive to 4-aminopyridine (0.3 mM), tetraethylammonium (1.7 mM), alpha-dendrotoxin (25 nM), noxiustoxin (200 nM), and mast cell degranulating peptide (200 nM). Thus, RCK2 is a non-inactivating delayed rectifier K+ channel with interesting pharmacological properties.

摘要

大鼠脑钾离子通道RCK家族的一个新成员，称为RCK2，已完成测序并在非洲爪蟾卵母细胞中表达。钾离子电流呈电压依赖性，在20毫秒内（0毫伏时）被激活，5秒内不发生失活，在蛙任氏液中的单通道电导为8.2皮安。与RCK家族的其他成员相比，RCK2的药理学特性独特，该通道对大蝎毒素（[(1988)美国国家科学院院刊85, 3329 - 3333]）的阻断具有抗性（半数抑制浓度IC50 = 3.3微摩尔），但对4 - 氨基吡啶（0.3毫摩尔）、四乙铵（1.7毫摩尔）、α - 树眼镜蛇毒素（25纳摩尔）、诺蝎毒素（200纳摩尔）和肥大细胞脱颗粒肽（200纳摩尔）相对敏感。因此，RCK2是一种具有有趣药理学特性的非失活延迟整流钾离子通道。