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首页> 外文期刊>American Journal of Physiology >Induction of rhythmic transient depolarizations associated with waxing and waning of slow wave activity in intestinal smooth muscle
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Induction of rhythmic transient depolarizations associated with waxing and waning of slow wave activity in intestinal smooth muscle

机译:诱导肠道平滑肌缓释和慢波活性的发布和衰落相关的节律瞬态去极化

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This motor pattern can arise when low-frequency transient depolarizations are evoked in the interstitial cells of Cajal associated with the deep muscular plexus (ICC-DMP) network, which then affect the omnipresent slow wave activity: changing its regular amplitude into a waxing and waning pattern. The objective of the present study was to investigate physiological stimuli that could induce the low-frequency component. Intracellular recordings were obtained from circular muscle with or without attached mucosa. Decanoic acid (1 mM) and butyric acid (10 mM) both evoked low-frequency transient depolarizations but through different mechanisms. Decanoic acid-induced waxing and waning was initiated by purely myogenic means when perfused onto exposed circular muscle. Butyric acid required the intact mucosa and uninhibited neural activity to elicit the low-frequency response. Evidence is provided that the transient rhythmic depolarizations occur in the absence of interstitial cells of Cajal associated with the myenteric plexus (ICC-MP). Onset of the slow transient depolarizations was stimulated by addition of A"-nitro-L-arginine (l-NNA; 100 p-M); thus the low-frequency component seems to be under chronic inhibition by nitric oxide. Excitatory tachykinergic stimulation induced the low-frequency component since substance P (0.5 pM) evoked it in the presence of neural blockade. In summary, interplay between two networks of myogenic pacemakers, neural activity, and nutrient factors such as fatty acids plays a role in the generation of the rhythmic low-frequency component that is essential for the development of the checkered segmentation motor pattern.
机译:当在与深肌法丛(ICC-DMP)网络相关的CAJAL的间质细胞中唤起低频瞬时去极化时,可以出现这种电动机图案,这会影响全峰慢波活动:将定期幅度变为打蜡和衰退图案。本研究的目的是研究可以诱导低频分量的生理刺激。从有或没有附着的粘膜的圆形肌肉获得细胞内记录。癸酸(1mM)和丁酸(10mm)均诱发低频瞬态去极化,但通过不同的机制。在灌注到暴露在暴露的圆形肌上时,通过纯粹的肌原型发起癸酸诱导的打蜡和衰退。丁酸需要完整的粘膜和不羁的神经活动,以引出低频响应。提供证据,即瞬态节律磷酸化在没有与神经丛(ICC-MP)相关的CAGAL的不带性细胞的情况下发生。通过加入“-Nitro-L-精氨酸(L-NNA; 100 PM)刺激慢速瞬时去极化的发作;因此,低频分量似乎是通过一氧化氮的慢性抑制。兴奋性的直肠有效刺激诱导低 - 由于物质p(0.5 pm)在神经封锁存在下唤起它。总之,两个肌遗传起搏器,神经活动和脂肪酸等营养因子之间的相互作用在节奏低的产生中起着作用 - 对方格分割电机模式开发至关重要的频率分量。

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