首页> 外文期刊>The Journal of Physiology >Morphological and functional changes in guinea-pig neurons projecting to the ileal mucosa at early stages after inflammatory damage.
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Morphological and functional changes in guinea-pig neurons projecting to the ileal mucosa at early stages after inflammatory damage.

机译:炎性损伤后早期向回肠粘膜投射的豚鼠神经元的形态和功能变化。

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摘要

In the present study the relationship between tissue damage and changed electro-physiological properties of Dogiel type II myenteric neurons within the first 24 hours after induction of inflammation with trinitrobenzene sulfonate (TNBS) in the guinea-pig ileum was investigated. Treatment with TNBS causes damage to the mucosa, inflammatory responses in the mucosa and enteric ganglia and changes in myenteric neuron properties. Thus we hypothesise that the physiological changes in the myenteric neurons could be due to damage to their mucosal processes or inflammation in the vicinity of cell bodies or the processes. We found an association between hyperexcitability of myenteric Dogiel type II neurons and damage to the mucosa and its innervation at 3 and 24 h, times when there was also an inflammatory reaction. The lack of hyperexcitability in neurons from control tissues in which axons projecting to the mucosa were severed suggests that inflammation may be an important contributing factor to the neuronal hyperexcitability at the acute stage of inflammation. Despite mucosal repair and re-innervation of the mucosa before 7 days after induction of inflammation, neuronal hyperexcitability persists. Although the mechanisms underlying neuronal hyperexcitability at the acute stage of inflammation might be different from those underlying long-term changes in the absence of active inflammation in the ganglia, the persistent changes in neuronal excitability may contribute to post-inflammatory gut dysfunctions.
机译:在本研究中,研究了豚鼠回肠中三硝基苯磺酸盐(TNBS)诱发炎症后的最初24小时内,组织损伤和II型Dogiel肠系膜神经元电生理特性之间的关系。 TNBS的治疗可引起粘膜损害,粘膜和肠神经节的炎症反应以及肌层神经元特性的改变。因此,我们假设肌层神经元的生理变化可能是由于其粘膜过程受损或细胞体或过程附近的炎症引起的。我们发现,在3和24小时(也有发炎反应的时间),II型门氏多毛犬神经元的过度兴奋性与对粘膜的损害及其神经支配之间存在关联。来自控制组织的神经元缺乏过度兴奋性,在控制组织中,轴突伸向粘膜已被切断,这表明炎症可能是炎症急性期神经元过度兴奋的重要因素。尽管在诱发炎症后7天之前进行了黏膜修复和黏膜再支配,但神经元过度兴奋仍然持续。尽管炎症急性期神经元过度兴奋的潜在机制可能与神经节中没有活动性炎症的长期变化的潜在机制不同,但神经元兴奋性的持续改变可能会导致炎症后肠道功能异常。

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