Discipline of Human Physiology and Centre for Neuroscience, Flinders University, Adelaide, Australia.
Am J Physiol Gastrointest Liver Physiol. 2011 Sep;301(3):G519-27. doi: 10.1152/ajpgi.00101.2011. Epub 2011 Jun 23.
The mechanisms underlying distension-evoked peristalsis in the colon are incompletely understood. It is well known that, following colonic distension, 5-hydroxytryptamine (5-HT) is released from enterochromaffin (EC) cells in the intestinal mucosa. It is also known that exogenous 5-HT can stimulate peristalsis. These observations have led some investigators to propose that endogenous 5-HT release from EC cells might be involved in the initiation of colonic peristalsis, following distension. However, because no direct evidence exists to support this hypothesis, the aim of this study was to determine directly whether release of 5-HT from EC cells was required for distension-evoked colonic peristalsis. Real-time amperometric recordings of 5-HT release and video imaging of colonic wall movements were performed on isolated segments of guinea pig distal colon, during distension-evoked peristalsis. Amperometric recordings revealed basal and transient release of 5-HT from EC cells before and during the initiation of peristalsis, respectively. However, removal of mucosa (and submucosal plexus) abolished 5-HT release but did not inhibit the initiation of peristalsis nor prevent the propagation of fecal pellets or intraluminal fluid. Maintained colonic distension by fecal pellets induced repetitive peristaltic waves, whose intrinsic frequency was also unaffected by removal of the submucosal plexus and mucosa, although their propagation velocities were slower. In conclusion, the mechanoreceptors and sensory neurons activated by radial distension to initiate peristalsis lie in the myenteric plexus and/or muscularis externa, and their activation does not require the submucosal plexus, release of 5-HT from EC cells, nor the presence of the mucosa. The propagation of peristalsis and propulsion of liquid or solid content along the colon is entrained by activity within the myenteric plexus and/or muscularis externa and does not require sensory feedback from the mucosa, nor neural inputs arising from submucosal ganglia.
目前，人们对于肠道扩张引发蠕动的机制仍知之甚少。众所周知，在结肠扩张后，肠嗜铬细胞（enterochromaffin cells，EC）会释放 5-羟色胺（5-hydroxytryptamine，5-HT）。此外，外源性 5-HT 可以刺激蠕动。这些观察结果促使一些研究人员提出，在结肠扩张后，EC 细胞释放的内源性 5-HT 可能参与了结肠蠕动的启动。然而，由于目前尚无直接证据支持这一假说，因此本研究旨在直接确定 EC 细胞释放 5-HT 是否是扩张引发的结肠蠕动所必需的。在豚鼠远端结肠的分离段上，通过实时电流记录法和结肠壁运动的视频成像，对扩张引发蠕动时的 5-HT 释放进行了研究。电流记录显示，在蠕动的启动前和启动时，EC 细胞分别出现基础和短暂的 5-HT 释放。然而，去除黏膜（和黏膜下丛）会消除 5-HT 释放，但不会抑制蠕动的启动，也不会阻止粪便颗粒或腔内液体的传播。粪便颗粒维持的结肠扩张会引发重复性蠕动波，尽管去除黏膜下丛和黏膜后，其固有频率不受影响，但蠕动波的传播速度会变慢。总之，径向扩张激活的机械感受器和感觉神经元位于肌间神经丛和/或外肌层，其激活不需要黏膜下丛、EC 细胞释放 5-HT，也不需要黏膜的存在。蠕动的传播和液体或固体内容物沿结肠的推进是由肌间神经丛和/或外肌层的活动引起的，不需要黏膜的感觉反馈，也不需要来自黏膜下神经节的神经输入。
