Kito Yoshihiko, Suzuki Hikaru, Edwards Frank R
Department of Physiology, Nagoya City University Medical School, Mizuho-ku, Nagoya 467-8601, Japan.
J Smooth Muscle Res. 2002 Dec;38(6):165-79. doi: 10.1540/jsmr.38.165.
Intracellular recordings were made from myenteric interstitial cells of Cajal (ICC-MY) distributed in the guinea-pig gastric antrum to investigate the properties of unitary potentials. In most cells studied, pacemaker potentials with initial fast transient and following plateau components were generated periodically, and intervals between the potentials were quiescent. However, there were few cells (less than 5% of cells examined) which showed discharge of unitary potentials spontaneously in the intervals between pacemaker potentials. The amplitude and frequency of unitary potentials appeared to be random variables, as observed in isolated circular smooth muscle bundles of the guinea-pig gastric antrum. BAPTA-AM (an intracellular Ca2+ chelator) or papaverine (a non-selective phosphodiesterase inhibitor) reduced the discharge frequency of unitary potentials, with associated decrease in the frequency of pacemaker potentials. These agents finally abolished both unitary potentials and pacemaker potentials. In preparations showing no detectable generation of unitary potentials, depolarization of the membrane with high-K solution ([K+]o = 10.6 mM) elicited generation of unitary potentials during intervals between pacemaker potentials. Pinacidil (an opener of K(ATP)-channels) hyperpolarized the membrane and increased the frequency and amplitude of unitary potentials with no alteration to the relationship between the amplitudes of unitary potentials and their half-widths. These results suggest that the elevation of intracellular Ca2+ concentration is causally related to the generation of unitary potentials in pacemaker cells. They are consistent with the proposition that the depolarization produced by a burst of unitary potentials triggers the primary component of pacemaker potentials in ICC-MY, which induces a release of Ca2+ from inositol 1,4,5-trisphosphate (IP3)-sensitive internal stores and then activates Ca2+-sensitive Cl- -channels to form the plateau component. Similarities and differences in unitary potentials between circular muscle and pacemaker cells are discussed.
通过对豚鼠胃窦中分布的肌间 Cajal 间质细胞(ICC-MY)进行细胞内记录,以研究单一电位的特性。在大多数被研究的细胞中,具有初始快速瞬变和随后平台成分的起搏电位周期性产生,电位之间的间隔是静止的。然而,很少有细胞(在所检查细胞中少于 5%)在起搏电位之间的间隔中自发显示单一电位放电。单一电位的幅度和频率似乎是随机变量,这与在豚鼠胃窦分离的环形平滑肌束中观察到的情况一样。BAPTA-AM(一种细胞内 Ca2+螯合剂)或罂粟碱(一种非选择性磷酸二酯酶抑制剂)降低了单一电位的放电频率,同时起搏电位频率也随之降低。这些药物最终消除了单一电位和起搏电位。在未检测到单一电位产生的标本中,用高钾溶液([K+]o = 10.6 mM)使膜去极化可在起搏电位之间的间隔期间引发单一电位的产生。吡那地尔(一种 K(ATP)通道开放剂)使膜超极化,并增加了单一电位的频率和幅度,而单一电位幅度与其半高宽之间的关系未改变。这些结果表明,细胞内 Ca2+浓度的升高与起搏细胞中单一电位的产生存在因果关系。它们与以下观点一致:单一电位爆发产生的去极化触发 ICC-MY 中起搏电位的主要成分,这会诱导从肌醇 1,4,5-三磷酸(IP3)敏感的内部储存中释放 Ca2+,然后激活 Ca2+敏感的 Cl-通道以形成平台成分。文中讨论了环形肌和起搏细胞之间单一电位的异同。