Kito Yoshihiko, Suzuki Hikaru
Department of Physiology, Nagoya City University Medical School, Mizuho-ku, Nagoya 467-8601, Japan.
J Physiol. 2003 Dec 15;553(Pt 3):803-18. doi: 10.1113/jphysiol.2003.051334. Epub 2003 Oct 17.
Recording of electrical responses from isolated small intestine of mice using conventional microelectrodes revealed two types of potential, a pacemaker potential and a slow wave, both with rapid rising primary components and following plateau components. The rate of rise and peak amplitude were greater for pacemaker potentials than for slow waves, and the plateau component was smaller in slow waves than in pacemaker potentials. Both potentials oscillated at a similar frequency (20-30 min-1). Unitary potentials often discharged during the interval between pacemaker potentials. Infusion of Lucifer Yellow allowed visualization of the recorded cells; pacemaker potentials were recorded from myenteric interstitial cells of Cajal (ICC-MY) while slow waves were recorded from circular smooth muscle cells. Pacemaker potentials were characterized as follows: the primary component was inhibited by Ni2+, Ca2+-free solution or depolarization with high-K+ solution, the plateau component was inhibited by 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS), an inhibitor of Ca2+-activated Cl- channels, low [Cl-]o solution or Ca2+-free solution, and the generation of potentials was abolished by co-application of Ni2+and DIDS or by chelating intracellular Ca2+ with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid acetoxymethyl ester (BAPTA-AM). These results indicate that in the mouse small intestine ICC-MY generate pacemaker potentials with two components in situ; the primary and plateau components may be generated by activation of voltage-dependent Ca2+-permeable channels and Ca2+-activated Cl- channels, respectively. Slow waves are generated in circular smooth muscles via electrotonic spread of pacemaker potentials. These properties of intestinal pacemaker potentials are considered essentially similar to those of gastric pacemaker potentials.
使用传统微电极记录小鼠离体小肠的电反应,发现有两种电位,即起搏电位和慢波,二者均具有快速上升的初级成分和随后的平台成分。起搏电位的上升速率和峰值幅度大于慢波,慢波的平台成分小于起搏电位。两种电位均以相似的频率振荡(20 - 30次/分钟)。在起搏电位的间隔期间,单一电位经常发放。注入荧光黄可使记录的细胞可视化;起搏电位是从肌间 Cajal 间质细胞(ICC - MY)记录到的,而慢波是从环行平滑肌细胞记录到的。起搏电位的特征如下:初级成分受到 Ni2 +、无 Ca2 +溶液或高 K +溶液去极化的抑制,平台成分受到 4,4'-二异硫氰基芪 - 2,2'-二磺酸(DIDS,一种 Ca2 +激活的 Cl - 通道抑制剂)、低[Cl - ]o溶液或无 Ca2 +溶液的抑制,同时应用 Ni2 +和 DIDS 或用 1,2 - 双(2 - 氨基苯氧基)乙烷 - N,N,N',N'-四乙酸乙酰甲酯(BAPTA - AM)螯合细胞内 Ca2 +可消除电位的产生。这些结果表明,在小鼠小肠中,ICC - MY 在原位产生具有两种成分的起搏电位;初级成分和平台成分可能分别由电压依赖性 Ca2 +通透通道和 Ca2 +激活的 Cl - 通道的激活所产生。慢波是通过起搏电位的电紧张性扩布在环行平滑肌中产生的。肠道起搏电位的这些特性被认为与胃起搏电位的特性基本相似。