Yoneda Satoshi, Takano Hiromichi, Takaki Miyako, Suzuki Hikaru
Department of Physiology, Nagoya City University Medical School, Japan.
J Smooth Muscle Res. 2003 Jun;39(3):55-65. doi: 10.1540/jsmr.39.55.
The effects of nifedipine and nickel ions (Ni2+), known inhibitors of L- and T-type voltage-gated Ca-channels respectively, were investigated on plateau potentials recorded from submucosal interstitial cells distributed in the mouse proximal colon. Plateau potentials were generated at a frequency of about 15 times min(-1) and were formed of two components. The primary component had an initial fast rate of rise with a transient potential (rate of rise, 130 mV/s; peak amplitude, 35 mV) and was followed by a secondary plateau component with a sustained potential (amplitude, 25 mV; duration, 2.6 s). Each cell from which recordings were made was injected with neurobiotin. Subsequent morphological examination with a confocal microscope indicated successful visualization of injected cells only in the presence of 18beta-glycylrhetinic acid (an inhibitor of gap junctional connections), suggesting that these cells were dye-coupled with surrounding cells. The cells injected with neurobiotin exhibited an oval-shaped cell body with bipolar processes and were distributed in the submucosal layer, suggesting that they were submucosal interstitial cells of Cajal (ICC-SM). The plateau potentials were not altered by 0.01 microM nifedipine, but were reduced in duration by 0.1 microM nifedipine, and abolished by 1 microM nifedipine. The rate of rise of plateau potentials, but not their amplitude, was reduced by Ni2+ (> 10 microM), with no significant alteration of the membrane potential. In the presence of 100 microM Ni2+, the plateau potentials were changed to a triangular form. Thus, the plateau potentials were formed by two types of voltage-gated channel current: the initial component was produced by a Ni2+-sensitive channel current and the plateau component by a nifedipine-sensitive current. The possible involvement of two different types of voltage-gated Ca2+-channels in the generation of submucosal pacemaker potentials was discussed.
分别作为L型和T型电压门控钙通道已知抑制剂的硝苯地平和镍离子（Ni2+），对从小鼠近端结肠分布的黏膜下间质细胞记录的平台电位的影响进行了研究。平台电位以约每分钟15次的频率产生，由两个成分组成。主要成分具有初始快速上升速率，伴有一个瞬态电位（上升速率为130 mV/s；峰值幅度为35 mV），随后是一个具有持续电位的次要平台成分（幅度为25 mV；持续时间为2.6 s）。对每个进行记录的细胞注射神经生物素。随后用共聚焦显微镜进行的形态学检查表明，仅在存在18β-甘氨酰维甲酸（一种缝隙连接抑制剂）的情况下，注射细胞才能成功可视化，这表明这些细胞与周围细胞存在染料偶联。注射神经生物素的细胞呈现出椭圆形细胞体，具有双极突起，分布在黏膜下层，表明它们是 Cajal 黏膜下间质细胞（ICC-SM）。0.01 μM 硝苯地平对平台电位无影响，但0.1 μM 硝苯地平使平台电位持续时间缩短，1 μM 硝苯地平则使其消失。Ni2+（>10 μM）降低了平台电位的上升速率，但不影响其幅度，膜电位无明显改变。在存在100 μM Ni2+的情况下，平台电位变为三角形。因此，平台电位由两种类型的电压门控通道电流形成：初始成分由对Ni2+敏感的通道电流产生，平台成分由对硝苯地平敏感的电流产生。文中讨论了两种不同类型的电压门控Ca2+通道在黏膜下起搏电位产生过程中可能的作用。
