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首页> 外文期刊>Life sciences >Enhancement of K 2P2.1 (TREK1) background currents expressed in Xenopus oocytes by voltage-gated K + channel β subunits
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Enhancement of K 2P2.1 (TREK1) background currents expressed in Xenopus oocytes by voltage-gated K + channel β subunits

机译：电压门控的K +通道β亚基增强在非洲爪蟾卵母细胞中表达的K 2P2.1（TREK1）背景电流

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Aims: K 2P2.1 (TREK1) two-pore-domain potassium channels control electrical activity in the central nervous system (CNS) and in the heart. Auxiliary β subunits (Kvβ) increase functional K + channel diversity in the CNS. Based on similar tissue distribution and common functional significance of Kvβ2 protein and K 2P2.1 channels in neuronal excitability, we hypothesized that Kvβ2 subunits modulate K 2P2.1 currents. Main methods: Rat K 2P2.1 channels and rKvβ subunits were expressed in Xenopus laevis oocytes, and two-electrode voltage clamp electrophysiology was used to assess K 2P2.1 function. Key findings: Kvβ2 subunits increased K 2P2.1 currents by 2.9-fold in concentration-dependent fashion (I 0mV,K2P2.1, 0.53 ± 0.07 μA; I 0mV,K2P2.1 + Kvβ2, 1.56 ± 0.13 μA; n = 15). K 2P2.1 channel stimulation resulted in resting membrane potential hyperpolarization by - 10.7 mV (n = 15). Open rectification and current-voltage relationships of K 2P2.1 channels were not markedly altered upon co-expression with Kvβ2, and K 2P2.1 membrane expression was not affected by Kvβ2 subunits. Related subunits Kvβ1 (1.7-fold; n = 16), Kvβ3 (2.2-fold; n = 16), and Kvβ4 (2.8-fold; n = 16) similarly activated K 2P2.1 currents, indicating a broader role for Kvβ proteins in K 2P2.1 regulation. Significance: Kvβ subunits stabilize the resting membrane potential through enhancement of K 2P2.1 K + currents. The significance of this previously unappreciated biophysical mechanism in neuronal physiology remains to be investigated.
机译：目的：K 2P2.1（TREK1）两孔域钾离子通道控制着中枢神经系统（CNS）和心脏的电活动。辅助β亚基（Kvβ）增加CNS中功能性K +通道的多样性。基于相似的组织分布以及Kvβ2蛋白和K 2P2.1通道在神经元兴奋性中的共同功能意义，我们假设Kvβ2亚基调节K 2P2.1电流。主要方法：在非洲爪蟾卵母细胞中表达大鼠K 2P2.1通道和rKvβ亚基，并用两电极电压钳电生理法评估K 2P2.1的功能。关键发现：Kvβ2亚基以浓度依赖性方式使K 2P2.1电流增加2.9倍（I 0mV，K2P2.1，0.53±0.07μA; I 0mV，K2P2.1 +Kvβ2，1.56±0.13μA; n = 15 ）。 K 2P2.1通道刺激导致静息膜电位超极化达-10.7 mV（n = 15）。与Kvβ2共表达时，K 2P2.1通道的开放整流和电流-电压关系没有明显改变，并且Kvβ2亚基不影响K 2P2.1膜表达。相关亚基Kvβ1（1.7倍; n = 16），Kvβ3（2.2倍; n = 16）和Kvβ4（2.8倍; n = 16）类似地激活K 2P2.1电流，表明Kvβ蛋白的作用更广泛在K 2P2.1法规中。意义：Kvβ亚基通过增强K 2P2.1 K +电流来稳定静息膜电位。这种以前未被认识的生物物理机制在神经元生理学中的重要性仍有待研究。

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