卡哈尔间质细胞
起搏器电位
去极化
补品(生理学)
运动性
神经科学
二氢吡啶
化学
生物
生物物理学
内分泌学
内科学
钙
医学
细胞生物学
平滑肌
作者
Kenton M. Sanders,Sang Don Koh,Sean M. Ward
出处
期刊:Annual Review of Physiology
[Annual Reviews]
日期:2006-01-01
卷期号:68 (1): 307-343
被引量:552
标识
DOI:10.1146/annurev.physiol.68.040504.094718
摘要
In the gastrointestinal tract, phasic contractions are caused by electrical activity termed slow waves. Slow waves are generated and actively propagated by interstitial cells of Cajal (ICC). The initiation of pacemaker activity in the ICC is caused by release of Ca2+ from inositol 1,4,5-trisphosphate (IP3) receptor-operated stores, uptake of Ca2+ into mitochondria, and the development of unitary currents. Summation of unitary currents causes depolarization and activation of a dihydropyridine-resistant Ca2+ conductance that entrains pacemaker activity in a network of ICC, resulting in the active propagation of slow waves. Slow wave frequency is regulated by a variety of physiological agonists and conditions, and shifts in pacemaker dominance can occur in response to both neural and nonneural inputs. Loss of ICC in many human motility disorders suggests exciting new hypotheses for the etiology of these disorders.
科研通智能强力驱动
Strongly Powered by AbleSci AI