Pacemaker potentials generated by interstitial cells of Cajal in the murine intestine
Pacemaker potentials generated by interstitial cells of Cajal in the murine intestine
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DOI：
10.1152/ajpcell.00361.2004
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发表时间：
2005-03-01
影响因子：
5.5
通讯作者：
Sanders, KM
中科院分区：
文献类型：
--
作者：
Kito, Y;Ward, SM;Sanders, KM
在小鼠小肠的Cajal肌间质细胞（ICC-MY）中原位记录起搏电位。研究了起搏电位的两个组成部分（上升和平台）的性质，并与环形肌细胞记录的慢波进行了比较。硝苯地平（3 μ M）不能阻断起搏电位和慢波。在硝苯地平存在下，电压依赖性钙通道阻滞剂米贝拉地尔以剂量依赖性方式（1 - 30 μ M）降低起搏电位和慢波的上行程去极化（dV/dt（max））的幅度、频率和上升速率。米贝拉地尔（30 μ M）改变了起搏电位的模式，从快速上升，高频事件缓慢去极化，低频事件与相当大的膜噪声（单一电位）之间的起搏电位。咖啡因（3毫米）废除起搏电位的存在下，米贝拉地尔。吡那地尔（10 μ M），一种ATP敏感的K+通道开放剂，使ICC-MY超极化，并增加振幅和dV/dt（max），而不影响频率。吡那地尔使平滑肌细胞超极化，并减弱慢波的振幅和dV/dt（max），而不影响频率。吡那地尔的作用被格列本脲（10 μ M）阻断。这些数据表明，慢波是由起搏电位驱动的电紧张电位。起搏器电位的上升成分是由于二氢吡啶抗性Ca 2+通道的激活，这种去极化引起起搏器活动以产生平台电位。平台电位可能是由于ICC-MY中单个或小组起搏器单元产生的单位电位的总和。单一电位的夹带似乎取决于上行程去极化过程中的Ca 2+进入。
Pacemaker potentials were recorded in situ from myenteric interstitial cells of Cajal (ICC-MY) in the murine small intestine. The nature of the two components of pacemaker potentials (upstroke and plateau) were investigated and compared with slow waves recorded from circular muscle cells. Pacemaker potentials and slow waves were not blocked by nifedipine ( 3 muM). In the presence of nifedipine, mibefradil, a voltage-dependent Ca2+ channel blocker, reduced the amplitude, frequency, and rate of rise of upstroke depolarization (dV/dt(max)) of pacemaker potentials and slow waves in a dose-dependent manner ( 1 - 30 muM). Mibefradil ( 30 muM) changed the pattern of pacemaker potentials from rapidly rising, high-frequency events to slowly depolarizing, low-frequency events with considerable membrane noise ( unitary potentials) between pacemaker potentials. Caffeine ( 3 mM) abolished pacemaker potentials in the presence of mibefradil. Pinacidil ( 10 muM), an ATP-sensitive K+ channel opener, hyperpolarized ICC-MY and increased the amplitude and dV/dt(max) without affecting frequency. Pinacidil hyperpolarized smooth muscle cells and attenuated the amplitude and dV/dt(max) of slow waves without affecting frequency. The effects of pinacidil were blocked by glibenclamide ( 10 muM). These data suggest that slow waves are electrotonic potentials driven by pacemaker potentials. The upstroke component of pacemaker potentials is due to activation of dihydropyridine-resistant Ca2+ channels, and this depolarization entrains pacemaker activity to create the plateau potential. The plateau potential may be due to summation of unitary potentials generated by individual or small groups of pacemaker units in ICC-MY. Entrainment of unitary potentials appears to depend on Ca2+ entry during upstroke depolarization.