Enhanced excitability of guinea pig ileum myenteric AH neurons during and following recovery from chemical colitis.
Enhanced excitability of guinea pig ileum myenteric AH neurons during and following recovery from chemical colitis.
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DOI：
10.1016/j.neulet.2013.04.021
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发表时间：
2013-06-17
影响因子：
2.5
通讯作者：
Linden DR
中科院分区：
文献类型：
--
作者：
Linden DR
结肠炎会改变胃肠道更近端区域的运动功能。结肠炎改变了炎症区域内肠神经元的神经生理学，这可能导致结肠运动和分泌功能的改变。这项研究试图验证一种假设，即结肠炎改变了非炎症回肠肌间神经元的神经生理学，并且神经生理学改变与小肠运动功能改变是一致的。三硝基苯磺酸(TNBS)诱导的结肠炎与回肠肌间神经丛AH神经元的过度兴奋有关，表现为神经元去极化和动作电位数量增加，但这些细胞的可塑性典型的动作电位时程或后超极化没有变化。本研究中观察到的AH神经元和S神经元的突触传递均未见改变。在给予TNBS后的24小时内，AH神经元开始出现高兴奋性，并持续到8周，即结肠炎缓解后的时间点。肠传输功能在TNBS后12h开始减少，48h后消失。虽然AH神经元在协调回肠运动功能中起着中心作用，但这些神经元兴奋性的变化与小肠运输的变化并不一致。
Inflammation of the colon changes motor function of more proximal regions of the gastrointestinal tract. Colitis alters the neurophysiology of enteric neurons within the region of inflammation, which may contribute to altered colonic motor and secretory function. This study seeks to test the hypothesis that colitis alters the neurophysiology of myenteric neurons in the non-inflamed ileum, and that altered neurophysiology coincides with altered small bowel motor function. Trinitrobenzene sulfonic acid (TNBS)-induced colitis was associated with hyperexcitability of AH neurons in the ileum myenteric plexus, demonstrated by depolarized neurons and increased numbers of action potentials, but without changes in the action potential duration or afterhyperpolarization typical of plasticity in these cells. There were no changes in synaptic transmission of either AH neurons or S neurons observed in the current study. The onset of AH neuron hyperexcitability occurred 24h following administration of TNBS, and persisted to eight weeks, a time point following the resolution of colitis. Small bowel transit was reduced as early as 12h after TNBS and resolved by 48h after TNBS. While AH neurons play a central role in coordinating motor function of the ileum, changes in excitability of these neurons did not coincide with changes in small bowel transit.
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