Two modes of enteric gliotransmission differentially affect gut physiology.
Two modes of enteric gliotransmission differentially affect gut physiology.
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作者：
Grubišić V;Parpura V
肠神经系统(ENS)中的肠胶质细胞(EG)可以调节神经调节的肠道功能。利用分子遗传学，我们评估了在EG中表达的分子实体以及以其他方式介导的两种截然不同的胶质递质释放机制--连接蛋白43(Cx43)半通道和依赖钙的胞吐作用--对肠道功能的影响。突变的Cx43G138R在EG中的表达(它有利于半通道，而不是缝隙连接活性)在体内增加了肠道动力，而Cx43在EG中的敲除导致了肠道动力的降低。然而，抑制EG中依赖于钙离子的胞吐作用并不影响体内的肠道运动；相反，它增加了粪便小球液体的含量。抑制EG中Cx43的表达或抑制钙依赖的胞吐对结肠移行运动复合体有影响，主要是降低体外收缩的频率和速度。因此，EG可以利用上述两种不同的神经胶质传递机制来不同地调节肠道反射。
Enteric glia (EG) in the enteric nervous system (ENS) can modulate neuronally regulated gut functions. Using molecular genetics, we assessed the effects that molecular entities expressed in EG and otherwise mediating two distinct mechanisms of gliotransmitter release, connexin 43 (Cx43) hemichannel vs. Ca2+-dependent exocytosis, have on gut function. The expression of mutated Cx43G138R (which favors hemichannel, as opposed to gap-junctional activity) in EG increased gut motility in vivo, while a knock-down of Cx43 in EG resulted in the reduction of gut motility. However, inhibition of Ca2+-dependent exocytosis in EG did not affect gut motility in vivo; rather, it increased the fecal pellet fluid content. Hampering either Cx43 expression or Ca2+-dependent exocytosis in EG had an effect on colonic migrating motor complexes, mainly decreasing frequency and velocity of contractions ex vivo. Thus, EG can differentially modulate gut reflexes using the above two distinct mechanisms of gliotransmission.