Greene Derek L, Hoshi Naoto
Department of Pharmacology, University of California, 360 Med Surge II, Irvine, CA, 92697, USA.
Department of Physiology and Biophysics, University of California, Irvine, USA.
Cell Mol Life Sci. 2017 Feb;74(3):495-508. doi: 10.1007/s00018-016-2359-y. Epub 2016 Sep 19.
Neuronal Kv7 channels underlie a voltage-gated non-inactivating potassium current known as the M-current. Due to its particular characteristics, Kv7 channels show pronounced control over the excitability of neurons. We will discuss various factors that have been shown to drastically alter the activity of this channel such as protein and phospholipid interactions, phosphorylation, calcium, and numerous neurotransmitters. Kv7 channels locate to key areas for the control of action potential initiation and propagation. Moreover, we will explore the dynamic surface expression of the channel modulated by neurotransmitters and neural activity. We will also focus on known principle functions of neural Kv7 channels: control of resting membrane potential and spiking threshold, setting the firing frequency, afterhyperpolarization after burst firing, theta resonance, and transient hyperexcitability from neurotransmitter-induced suppression of the M-current. Finally, we will discuss the contribution of altered Kv7 activity to pathologies such as epilepsy and cognitive deficits.
神经元Kv7通道构成了一种电压门控的非失活钾电流，即M电流。由于其特殊特性，Kv7通道对神经元的兴奋性具有显著调控作用。我们将讨论已被证明能大幅改变该通道活性的各种因素，如蛋白质与磷脂相互作用、磷酸化、钙以及多种神经递质。Kv7通道定位于控制动作电位起始和传播的关键区域。此外，我们将探讨由神经递质和神经活动调节的通道动态表面表达。我们还将聚焦于神经Kv7通道已知的主要功能：控制静息膜电位和动作电位发放阈值、设定发放频率、爆发发放后的超极化后电位、θ振荡以及神经递质诱导的M电流抑制所致的短暂性兴奋性增强。最后，我们将讨论Kv7活性改变对癫痫和认知缺陷等病理状况的影响。
