Changes in colonic motility and the electrophysiological properties of myenteric neurons persist following recovery from trinitrobenzene sulfonic acid colitis in the guinea pig
Changes in colonic motility and the electrophysiological properties of myenteric neurons persist following recovery from trinitrobenzene sulfonic acid colitis in the guinea pig
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DOI：
10.1111/j.1365-2982.2007.00986.x
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发表时间：
2007-12-01
影响因子：
3.5
通讯作者：
Mawe, G. M.
中科院分区：
文献类型：
--
作者：
Krauter, E. M.;Strong, D. S.;Mawe, G. M.
胃肠动力的持续变化常常伴随着结肠炎的缓解，其机制尚不清楚。三硝基苯磺酸(TNBS)引起的豚鼠结肠炎可降低推进运动的速度，引起AH神经元的过度兴奋，并诱导突触易化。环氧合酶-2(COX-2)抑制对运动和AH神经元的变化很敏感。这项调查的目的是确定在结肠炎恢复后，运动和神经生理学变化是否持续。在给予TNBS 8周后，进行炎症、结肠动力和肌间神经元细胞内电生理的评估，并与匹配的对照组进行比较。在TNBS治疗后56天，结肠中的髓过氧化物酶水平与对照水平相当。在这个时间点，单独使用TNBS或TNBS加COX-2抑制剂治疗后，结肠运动速度相对于对照组降低。此外，S神经元的AH神经元的电特性和快速突触电位与对照组有显著差异，与活动期炎症时检测到的结果相当。总之，这些数据表明，活动性结肠炎期间启动的肌间神经生理学改变长期存在，并为炎症性肠病缓解期间个体肠道功能改变提供了一种潜在的机制。
Persistent changes in gastrointestinal motility frequently accompany the resolution of colitis, through mechanisms that remain to be determined. Trinitrobenzene sulfonic acid (TNBS) colitis in the guinea pig decreases the rate of propulsive motility, causes hyperexcitability of AH neurons, and induces synaptic facilitation. The changes in motility and AH neurons are sensitive to cyclooxygenase-2 (COX-2) inhibition. The aim of this investigation was to determine if the motility and neurophysiological changes persist following recovery from colitis. Evaluations of inflammation, colonic motility and intracellular electrophysiology of myenteric neurons 8 weeks after TNBS administration were performed and compared to matched control conditions. Myeloperoxidase levels in the colons were comparable to control levels 56 days after TNBS treatment. At this time point, the rate of colonic motility was decreased relative to controls following treatment with TNBS alone or TNBS plus a COX-2 inhibitor. Furthermore, the electrical properties of AH neurons and fast synaptic potentials in S neurons were significantly different from controls and comparable to those detected during active inflammation. Collectively, these data suggest that altered myenteric neurophysiology initiated during active colitis persists long term, and provide a potential mechanism underlying altered gut function in individuals during remission from inflammatory bowel disease.