Eguchi Yuta, Kuwano Yuki, Okada Satoshi, Morino Hiroyuki, Hashimoto Kouichi
Department of Neurophysiology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Department of Pediatrics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Commun Biol. 2025 Jun 5;8(1):866. doi: 10.1038/s42003-025-08302-6.
Kcnq channels are low-threshold voltage-dependent K channels that generate M-currents, which regulate the peri-threshold membrane potential. Kcnq channels reportedly participate in band-pass frequency responses (i.e., resonance), but it remains largely unclear how they contribute to generating resonance. We examined resonance in HEK293 cells expressing mouse Kcnq2 and Kcnq3 (Kcnq2/3) using whole-cell recording. Kcnq2/3-expressing cells generated resonance-like frequency-dependent responses. Kcnh7 channels displayed a rapid opposing conductance change followed by slow activation in response to a depolarizing voltage step, properties thought to be necessary for inductor-like activity. However, Kcnq2/3 channels exhibited only slow activation. The lack of an opposing conductance change was caused by the absence of rapid Kcnq2/3 channel inactivation. These data suggest that core ion channel characteristics that cause resonance-like frequency responses are not uniform among ion channels. The opposing conductance change is not necessary for resonance-like frequency responses but is crucial for fine frequency tuning and oscillation.
Kcnq通道是产生M电流的低阈值电压依赖性钾通道，M电流可调节阈周膜电位。据报道，Kcnq通道参与带通频率响应（即共振），但它们如何促成共振在很大程度上仍不清楚。我们使用全细胞记录法研究了表达小鼠Kcnq2和Kcnq3（Kcnq2/3）的HEK293细胞中的共振现象。表达Kcnq2/3的细胞产生了类似共振的频率依赖性反应。Kcnh7通道在去极化电压阶跃时表现出快速的反向电导变化，随后是缓慢激活，这些特性被认为是类似电感器活动所必需的。然而，Kcnq2/3通道仅表现出缓慢激活。缺乏反向电导变化是由于Kcnq2/3通道缺乏快速失活所致。这些数据表明，引起类似共振频率反应的核心离子通道特性在离子通道之间并不统一。反向电导变化对于类似共振的频率反应不是必需的，但对于精细的频率调谐和振荡至关重要。
