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首页> 外文期刊>American Journal of Physiology >ICC pacing mechanisms in intact mouse intestine differ from those in cultured or dissected intestine.
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ICC pacing mechanisms in intact mouse intestine differ from those in cultured or dissected intestine.

机译：完整小鼠肠道中的ICC起搏机制与培养或解剖的肠道中的ICC起搏机制不同。

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摘要

Pacing of mouse intestine is driven by spontaneous activity of a network of interstitial cells of Cajal in the myenteric plexus (ICC-MP). So far, highly dissected circular muscle (CM) strips from control and mutant mice lacking ICC-MP and isolated, cultured ICC from newborn control mice were used to analyze its properties. Using intact circular and longitudinal segments of intestine, we recently reported that there were both significant similarities and differences between pacing studied in segments and from isolated, dissected tissues. Here, we report additional similarities and differences in our model from those in highly reduced systems. Similar to cultured or dissected intestine, blockade of sarcoplasmic-endoplasmic reticulum Ca(2+) pumps with thapsigargin or cyclopiazonic acid reduced pacing frequency, but thapsigargin was less effective than in isolated, cultured ICC. Moreover, inhibition of inositol 1,4,5-trisphosphate (IP(3)) receptors with xestospongin C, a putative inhibitor of IP(3) receptors, failed to affect pacing but successfully blocked increased pacing frequency by phorbol ester. 2-Aminoethoxy-diphenylborate, a putative blocker of IP(3)-mediated calcium release, caused a significant decrease in the amplitude and frequency of contractions. The mitochondrial uncoupler carbonyl cyanide p-trifluormethoxyphenylhydrazone blocked pacing and KCl-induced contractions at a concentration of 1 microM. The cyclic nucleotide agonists sodium nitroprusside (SNP), forskolin, and 8-bromo-cGMP inhibited pacing in CM. In longitudinal muscle (LM), SNP and forskolin had little effect on pacing. Furthermore, dibutyryl-cAMP did not affect pacing in CM or LM. These results suggest that pacing in intact intestine is under partly similar regulatory control as in more reduced systems. However, pacing in intact intestine is not affected by xestospongin C, which abolishes pacing in isolated, cultured ICC and exhibits attenuated responses to thapsigargin. Also, major differences between LM and CM suggest a separate pacemaker may drive LM.
机译：鼠肠的起搏是由肌间神经丛（ICC-MP）中Cajal的间质细胞网络的自发活动驱动的。到目前为止，从缺乏ICC-MP的对照小鼠和突变小鼠中分离出的高度分离的环形肌（CM）条以及从新生对照小鼠中分离，培养的ICC用于分析其特性。使用完整的肠道圆形和纵向节段，我们最近报告说，在节段中以及从分离的解剖组织中研究的起搏之间既有明显的相似性，也有差异。在这里，我们报告了模型与高度精简系统中模型的其他异同。类似于培养或解剖的肠，与thapsigargin或环吡唑酸的肌浆网-内质网Ca（2+）泵降低起搏频率，但thapsigargin比在分离的培养的ICC中效果差。此外，抑制肌醇1,4,5-三磷酸（IP（3））受体与xestospongin C，推定的IP（3）受体抑制剂，未能影响起搏，但成功地阻止了佛波酯的起搏频率。 2-氨基乙氧基二苯硼酸酯，IP（3）介导的钙释放的公认阻滞剂，引起收缩的幅度和频率的显着降低。线粒体解偶联剂羰基氰化物对-三氟甲氧基苯基blocked在1 microM的浓度下阻止起搏和KCl诱导的收缩。环状核苷酸激动剂硝普钠（SNP），毛喉素和8-溴-cGMP抑制CM的起搏。在纵向肌肉（LM）中，SNP和福司可林对起搏作用影响很小。此外，二丁酰-cAMP不影响CM或LM的起搏。这些结果表明，完整肠道中的起搏与部分简化的系统在部分类似的调节控制之下。但是，完整肠道中的起搏不受异源pongin C的影响，这可以消除分离的培养的ICC中的起搏，并且对毒胡萝卜素的反应减弱。而且，LM和CM之间的主要差异表明，单独的起搏器可能会驱动LM。

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