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介质细胞中的Ca2+动态:胃肠道运动模式的基本机制
Kenton M Sanders1, Bernard T Drumm2, Caroline A Cobine2
1Department of Physiology and Cell Biology, School of Medicine, University of Nevada-Reno, Reno, Nevada, United States.
Physiological reviews
|August 10, 2023
概括
卡哈尔 (ICC) 和PDGFRα+细胞的间歇细胞形成SIP同胞体,调节胃肠运动. 它们的Ca2+信号机制建议用"SIPgenic"代替"myogenic"来描述GI运动模式.
科学领域:
- 胃肠道生理学 胃肠道生理学
- 细胞电生理学 细胞电生理学
- 顺滑肌肉生物学 顺滑肌肉生物学
背景情况:
- 胃肠道 (GI) 运动依赖于光滑肌细胞 (SMC) 和间歇细胞.
- 间歇性细胞,包括ICC和PDGFRα+细胞,形成SIP同胞体,调整SMC刺激性并产生心脏起器活动.
- 这些细胞利用由细胞内Ca2+释放调节的Ca2+依赖导电量.
研究的目的:
- 审查Ca2+处理机制在间歇性细胞中调节肠道动性的作用.
- 提出一个新的术语",SIPgenic",以取代"myogenic"在描述GI运动模式.
- 突出SIP syncytium在肠道运动控制中的重要性.
主要方法:
- 对间歇细胞,Ca2+信号传递和肠道动性现有文献的综述.
- 分析Ca2+过渡物,导电量 (Ano1,Kcnn3) 以及它们对SMC刺激性的影响.
- 讨论神经传递对Ca2+信号传递和SIP syncytium通信的影响.
主要成果:
- 通过Ano1通道,ICC产生自发的短暂向内流和脱极化.
- 在Ca2+释放的影响下,PDGFRα+细胞通过Kcnn3通道产生向外流.
- 神经递质调节Ca2+过渡体,影响SIP同胞体活动和胃肠道运动模式.
结论:
- 介质细胞中Ca2+的处理是GI运动的核心.
- 术语"SIPgenic"更好地反映了SIP syncytium对GI运动模式的贡献,而不是"myogenic".
- 了解这些机制对于理解肠道功能和功能障碍至关重要.
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