Abstract：
Gastrointestinal (GI) organs display spontaneous, non-neurogenic electrical, and mechanical rhythmicity that underlies fundamental motility patterns, such as peristalsis and segmentation. Electrical rhythmicity (aka slow waves) results from pacemaker activity generated by interstitial cells of Cajal (ICC). ICC express a unique set of ionic conductances and Ca2+ handling mechanisms that generate and actively propagate slow waves. GI smooth muscle cells lack these conductances. Slow waves propagate actively within ICC networks and conduct electrotonically to smooth muscle cells via gap junctions. Slow waves depolarize smooth muscle cells and activate voltage-dependent Ca2+ channels (predominantly CaV1.2), causing Ca2+ influx and excitation-contraction coupling. The main conductances responsible for pacemaker activity in ICC are ANO1, a Ca2+ -activated Cl- conductance, and CaV3.2. The pacemaker cycle, as currently understood, begins with spontaneous, localized Ca2+ release events in ICC that activate spontaneous transient inward currents due to activation of ANO1 channels. Depolarization activates CaV 3.2 channels, causing the upstroke depolarization phase of slow waves. The upstroke is transient and followed by a long-duration plateau phase that can last for several seconds. The plateau phase results from Ca2+ -induced Ca2+ release and a temporal cluster of localized Ca2+ transients in ICC that sustains activation of ANO1 channels and clamps membrane potential near the equilibrium potential for Cl- ions. The plateau phase ends, and repolarization occurs, when Ca2+ stores are depleted, Ca2+ release ceases and ANO1 channels deactivate. This review summarizes key mechanisms responsible for electrical rhythmicity in gastrointestinal organs.
摘要：
胃肠道（GI）器官显示自发，非神经源性电，和基本运动模式的机械节律，如蠕动和分割。电节律性（又称慢波）是由Cajal（ICC）间质细胞产生的起搏器活动引起的。ICC表达了一组独特的离子电导和Ca2处理机制，可产生并主动传播慢波。GI平滑肌细胞缺乏这些电导。慢波在ICC网络内积极传播，并通过间隙连接电传导到平滑肌细胞。慢波去极化平滑肌细胞并激活电压依赖性Ca2+通道（主要是CaV1.2），引起Ca2+流入和激发-收缩耦合。ICC中负责起搏器活动的主要电导是ANO1，即Ca2激活的Cl-电导，和CaV3.2.起搏器周期,正如目前所理解的，从自发开始，ICC中的局部Ca2释放事件，由于ANO1通道的激活而激活自发的瞬态内向电流。去极化激活CaV3.2通道,导致慢波的上冲程去极化阶段。上冲程是短暂的，然后是长时间的平稳阶段，可以持续几秒钟。平台期是由Ca2诱导的Ca2释放和ICC中局部Ca2瞬变的时间簇引起的，这些瞬时簇维持ANO1通道的激活并将膜电位夹在Cl-离子的平衡电位附近。高原阶段结束,复极化发生，当Ca2+储存耗尽时，Ca2+释放停止并且ANO1通道失活。这篇综述总结了胃肠道器官电节律性的关键机制。
