Takayama Ichiro, Horiguchi Kazuhide, Daigo Yataro, Mine Tetsuya, Fujino Masayuki A, Ohno Shinichi
Department of Anatomy, Yamanashi Medical University School of Medicine, Japan.
Arch Histol Cytol. 2002 Mar;65(1):1-26. doi: 10.1679/aohc.65.1.
In spite of a claim by Kobayashi (1990) that they do not correspond to the cells originally depicted by CAJAL, a particular category of fibroblast-like cells have been identified in the gut by electron microscopy (Faussone-Pellegrini, 1977; Thuneberg, 1980) and by immunohistochemistry for Kit protein (Maeda et al., 1992) under the term of the "interstitial cells of Cajal (ICC)". Generating electrical slow waves, the ICC are intercalated between the intramural neurons and the effector smooth muscular cells, to form a gastroenteric pacemaker system. ICC at the level of the myenteric plexus (IC-MY) are multipolar cells forming a reticular network. The network of IC-MY which is believed to be the origin of electrical slow waves is morphologically independent from but associated with the myenteric plexus. On the other hand, intramuscular ICC (IC-IM) usually have spindle-shaped contours arranged in parallel with the bulk smooth muscle cells. Associated with nerve bundles and blood vessels, the IC-IM possess receptors for neurotransmitters and such circulating hormones as cholecystokinin, suggesting their roles in neuromuscular and hormone-muscular transmissions. In addition, gap junctions connect the IC-MY and IC-IM, thereby realizing the electrically synchronized integrity of ICC as a pacemaker system in the gut. The smooth muscle cells are also coupled with ICC via gap junctions, and the functional unit thus formed enables rhythmically synchronized contractions and relaxations. It has recently been found that a lack of Kit-expressing cells may induce hyper-contractility of the tunica muscularis in vitro, whereas a decrease in Kit expression within the muscle wall causes dysmotility-like symptoms in vivo. The pacemaker system in the gut thus seems to play a critical role in the maintenance of both moderate and normal motility of the digestive tract. A loss of Kit positive cells has been detected in several diseases with an impaired motor activity, including diabetic gastroenteropathy. Pathogenesis of these diseases is thought to be accounted for by impaired slow waves and neuromuscular transmissions; a pacemaker disorder may possibly induce a dysmotility-like symptom called 'gastroenteric arrhythmia'. A knowledge of the structure and function of the ICC and the pacemaker system provides a basis for clarifying the normal mechanism and the pathophysiology of motility in the digestive tract.
尽管小林（1990年）声称它们与CAJAL最初描绘的细胞不对应，但通过电子显微镜（福索内 - 佩莱格里尼，1977年；图内伯格，1980年）以及针对Kit蛋白的免疫组织化学方法（前田等人，1992年），在肠道中已鉴定出一类特定的成纤维细胞样细胞，被称为“Cajal间质细胞（ICC）”。ICC产生电慢波，插在壁内神经元和效应器平滑肌细胞之间，形成胃肠起搏器系统。肌间神经丛水平的ICC（IC - MY）是形成网状网络的多极细胞。据信是电慢波起源的IC - MY网络在形态上独立于肌间神经丛，但与之相关。另一方面，肌内ICC（IC - IM）通常具有与大部分平滑肌细胞平行排列的纺锤形轮廓。IC - IM与神经束和血管相关联，拥有神经递质以及胆囊收缩素等循环激素的受体，表明它们在神经肌肉和激素 - 肌肉传递中发挥作用。此外，缝隙连接连接IC - MY和IC - IM，从而实现ICC作为肠道起搏器系统的电同步完整性。平滑肌细胞也通过缝隙连接与ICC相连，由此形成的功能单元能够实现有节律的同步收缩和舒张。最近发现，缺乏表达Kit的细胞可能在体外诱导肌层过度收缩，而肌壁内Kit表达的减少在体内会导致类似动力障碍的症状。因此，肠道中的起搏器系统似乎在维持消化道适度和正常的动力方面起着关键作用。在包括糖尿病性胃肠病在内的几种运动功能受损的疾病中，已检测到Kit阳性细胞的缺失。这些疾病的发病机制被认为是由慢波和神经肌肉传递受损所致；起搏器功能障碍可能会诱发一种称为“胃肠心律失常”的类似动力障碍的症状。对ICC和起搏器系统的结构与功能的了解为阐明消化道动力的正常机制和病理生理学提供了基础。
