Nakayama Shinsuke, Shimono Ken, Liu Hong-Nian, Jiko Hideyasu, Katayama Noburu, Tomita Tadao, Goto Kazunori
Department of Cell Physiology, Nagoya University Graduate School of Medicine, 65 Tsuruma-cho, Showa-ku, Nagoya 466-8550, Japan.
J Physiol. 2006 Nov 1;576(Pt 3):727-38. doi: 10.1113/jphysiol.2006.118893. Epub 2006 Sep 21.
Gastrointestinal (GI) motility is well organized. GI muscles act as a functional syncytium to achieve physiological functions under the control of neurones and pacemaker cells, which generate basal spontaneous pacemaker electrical activity. To date, it is unclear how spontaneous electrical activities are coupled, especially within a micrometre range. Here, using a microelectrode array, we show a spatio-temporal analysis of GI spontaneous electrical activity. The muscle preparations were isolated from guinea-pig stomach, and fixed in a chamber with an array of 8 x 8 planar multielectrodes (with 300 microm in interpolar distance). The electrical activities (field potentials) were simultaneously recorded through a multichannel amplifier system after high-pass filtering at 0.1 Hz. Dihydropyridine Ca(2+) channel antagonists are known to differentiate the electrical pacemaker activity of interstitial cells of Cajal (ICCs) by suppressing smooth muscle activity. In the presence of nifedipine, we observed spontaneous electrical activities that were well synchronized over the array area, but had a clear phase shift depending on the distance. The additional application of tetrodotoxin (TTX) had little effect on the properties of the electrical activity. Furthermore, by constructing field potential images, we visualized the synchronization of pacemaker electrical activities resolving phase shifts that were measurable over several hundred micrometres. The results imply a phase modulation mechanism other than neural activity, and we postulate that this mechanism enables smooth GI motility. In addition, some preparations clearly showed plasticity of the pacemaker phase shift.
胃肠道(GI)运动是高度有序的。胃肠道肌肉作为一个功能合体,在神经元和起搏细胞的控制下实现生理功能,这些细胞会产生基础自发性起搏电活动。迄今为止,尚不清楚自发性电活动是如何耦合的,尤其是在微米范围内。在这里,我们使用微电极阵列展示了胃肠道自发性电活动的时空分析。肌肉标本取自豚鼠胃,固定在一个带有8×8平面多电极阵列(极间距离为300微米)的腔室中。在0.1赫兹高通滤波后,通过多通道放大器系统同时记录电活动(场电位)。已知二氢吡啶Ca(2+)通道拮抗剂可通过抑制平滑肌活动来区分 Cajal间质细胞(ICC)的电起搏活动。在硝苯地平存在的情况下,我们观察到自发电活动在阵列区域内高度同步,但根据距离有明显的相位偏移。额外施加河豚毒素(TTX)对电活动特性影响不大。此外,通过构建场电位图像,我们可视化了起搏电活动的同步情况,解析了在几百微米范围内可测量的相位偏移。结果暗示了一种不同于神经活动的相位调制机制,我们推测这种机制有助于胃肠道的平稳运动。此外,一些标本清楚地显示了起搏相位偏移的可塑性。