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激活的大鼠小胶质细胞中诱导产生的延迟整流钾电流设定了静息膜电位。

Delayed rectifier potassium currents induced in activated rat microglia set the resting membrane potential.

作者信息

Chung S, Joe E, Soh H, Lee M Y, Bang H W

机构信息

Department of Physiology, Chung-Ang University College of Medicine, Seoul, South Korea.

出版信息

Neurosci Lett. 1998 Feb 13;242(2):73-6. doi: 10.1016/s0304-3940(98)00029-9.

DOI:10.1016/s0304-3940(98)00029-9
PMID:9533397
Abstract

The delayed rectifying outward K+ (IK) current was measured in lipopolysaccharide (LPS)-activated cultured rat microglial cells by using whole-cell patch clamp method. The current showed 'window current' where channels were available for activation but never fully inactivated. At near resting membrane potential some part of the current was able to be activated by depolarization. Among the several K+ channel blockers tested, only 4-aminopyridine (4-AP) was able to block most of the current and depolarize the membrane potential reversibly. These results suggest that 4-AP sensitive IK current plays a direct role of setting the resting membrane potential in LPS-activated microglia.

摘要

采用全细胞膜片钳方法,在脂多糖(LPS)激活的大鼠小胶质细胞中测量延迟整流外向K⁺(IK)电流。该电流呈现“窗电流”,即通道可被激活,但从未完全失活。在接近静息膜电位时,部分电流能够被去极化激活。在所测试的几种K⁺通道阻滞剂中,只有4-氨基吡啶(4-AP)能够阻断大部分电流并使膜电位可逆地去极化。这些结果表明,4-AP敏感的IK电流在LPS激活的小胶质细胞中对设定静息膜电位起直接作用。

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