Wood J D, Brann L R, Vermillion D L
Dig Dis Sci. 1986 Jun;31(6):638-50. doi: 10.1007/BF01318696.
These studies were directed toward better characterization of the abnormalities of motor function in the large intestine of mutant mice with congenital aganglionosis and megacolon. Analysis of pressure-volume relations in the megacolon and aganglionic terminal segment showed increased intestinal wall compliance in the dilated colon and reduced wall compliance in the aganglionic region as compared to normal littermates. Migrating contractile complexes occurred spontaneously in ganglionated regions of the large intestine of both normal and mutant mice, but never propagated into the aganglionic segment of the abnormal bowel. Tetrodotoxin eliminated the migrating complexes and increased random spontaneous contractions in all areas except the aganglionic region. Circular muscle tension was reduced by electrical field stimulation, and poststimulus rebound contractions occurred in all ganglionated regions of the intestine of both normal and mutant mice. No responses to electrical stimulation occurred in the aganglionic segments of the preparations from mutant mice. The poststimulus responses "fatigued" at a faster rate in the megacolonic region of the abnormal bowel than in the equivalent region of the normal bowel, when evoked repetitively over prolonged time periods. There were no differences between the intestines of normal and mutant mice in latency, amplitude, duration, or area under the contractile curves of the poststimulus responses. Intracellular electrical recording from circular muscle fibers revealed slow depolarizing potentials with action potentials at the crests in all regions of the large bowel from both normal and abnormal mice. It also showed excitatory and inhibitory junction potentials in response to electrical stimulation. Inhibitory junction potentials summated during repetitive stimulation and postinhibitory rebound excitation occurred after offset of the stimulation. Stimulus-evoked junction potentials were recorded in all regions of the large intestine except in the aganglionic segment of the mutant mice. We concluded that most of the electrical and mechanical behavior of the aganglionic terminal segment reflected the absence of inhibitory innervation of the musculature in this region.
这些研究旨在更好地描述患有先天性神经节缺失和巨结肠的突变小鼠大肠运动功能异常的特征。对巨结肠和无神经节终末段的压力-容积关系分析表明，与正常同窝小鼠相比，扩张结肠的肠壁顺应性增加，而无神经节区域的肠壁顺应性降低。正常和突变小鼠大肠的神经节化区域均自发出现移行性收缩复合体，但从未传播至异常肠段的无神经节部分。河豚毒素消除了移行性复合体，并增加了除无神经节区域外所有区域的随机自发收缩。电场刺激可降低环行肌张力，正常和突变小鼠肠道的所有神经节化区域均出现刺激后反弹收缩。突变小鼠制备物的无神经节段对电刺激无反应。当在较长时间内重复诱发时，异常肠段巨结肠区域刺激后反应的“疲劳”速度比正常肠段的等效区域更快。正常和突变小鼠肠道在刺激后反应的潜伏期、幅度、持续时间或收缩曲线下面积方面没有差异。对环行肌纤维进行细胞内电记录显示，正常和异常小鼠大肠所有区域的慢去极化电位在波峰处伴有动作电位。记录还显示，对电刺激有兴奋性和抑制性突触后电位。抑制性突触后电位在重复刺激时总和，刺激停止后出现抑制后反弹兴奋。除突变小鼠的无神经节段外，在大肠所有区域均记录到刺激诱发的突触后电位。我们得出结论，无神经节终末段的大多数电和机械行为反映了该区域肌肉组织缺乏抑制性神经支配。
