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首页> 外文会议>International Symposium on Cell/Tissue Injury and Cytoprotection/Organoprotection: Focus on GI Tract >Neurobiology of Corticotropin-Releasing Factor in the Enteric Nervous System during Stress
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Neurobiology of Corticotropin-Releasing Factor in the Enteric Nervous System during Stress

机译：压力肠道神经系统中皮质甾醇释放因子的神经生物学

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Stress is associated with the onset, exacerbation, and reactivation of many gastrointestinal disorders, including irritable bowel syndrome (IBS) and inflammatory bowel diseases (IBD). Corticotropin-releasing factor (CRF) is a neuropeptide that plays a major role in the body's overall responses to stress, including in the gut. The role of central CRF signaling pathways in stress-induced changes in gut motility has been well characterized. Recent studies suggest that peripheral CRF-related mechanisms also contribute to stress-induced changes in gut motility and intestinal mucosal function. CRF peptides (including CRF, urocortin 1,2, and 3) and CRF receptors (i.e. CRF_1 and CRF_2) are present in the gut, especially in the enteric nervous system (ENS). CRF and urocortin 1 increase the excitability of ENS neurons via activation of CRFt receptors expressed by the neurons. Peripheral administration of CRF or urocortin 1 inhibits gastric emptying and motility through interaction with CRF_2 receptors in the stomach and stimulates colonic transit, motility and defecation via activation of CRFt receptors in the large intestine. The changes in gastrointestinal motility induced by peripheral CRF or urocortin 1 mimic those induced by acute stress. Moreover, peripheral injection of CRF receptor antagonists, which do not cross the blood-brain barrier, prevents acute stress-induced delayed gastric emptying and stimulation of colonic motor function. Acute stress, peripheral CRF and the selective CRF_1 receptor agonist increase the excitability of neurons in the colonic myenteric plexus. Acute and chronic stress increase intestinal ion secretion and mucosal permeability to macromolecules and cause diarrhea. Effects of stress on intestinal mucosal function are mimicked by peripheral injection of CRF and are suppressed by peripheral injection of nonselective peptide CRF receptor antagonists. Findings of this nature are strong evidence that activation of peripheral CRF receptors in the ENS is an important mechanism involved in stress-related alterations of gut motility and mucosal function.
机译：应激与许多胃肠道疾病的发病，加重和再活化有关，包括肠易肠综合征（IBS）和炎性肠病（IBD）。皮质培素释放因子（CRF）是一种神经肽，其在身体对压力的整体反应中发挥着重要作用，包括肠道。中央CRF信号传导途径在肠道运动中的应力诱导变化中的作用得到了很好的表征。最近的研究表明外周CRF相关机制也有助于肠道运动和肠粘膜功能的应激诱导的变化。在肠道中存在CRF肽（包括CRF，UROCOOCORIN 1,2和3）和CRF受体（即CRF_1和CRF_2），特别是在肠道神经系统（ENS）中。 CRF和Urocortin 1通过激活神经元表达的Crft受体增加Ena神经元的兴奋性。 CRF或尿道素1的外周施用通过与胃中的CRF_2受体相互作用来抑制胃排空和动力，并通过在大肠中的CRFT受体激活刺激结肠转运，运动和排便。外周CRF或尿道素诱导的胃肠运动诱导的变化模拟急性胁迫诱导的那些。此外，外周注射CRF受体拮抗剂，不穿过血脑屏障，防止急性应激诱导的延迟胃排空和结肠运动功能的刺激。急性胁迫，外周CRF和选择性CRF_1受体激动剂增加了结肠神经元在结肠神经元中神经元的兴奋性。急性和慢性应激增加肠道离子分泌和对大分子的粘膜渗透性并引起腹泻。应力对肠粘膜功能的影响是通过外周注射CRF的模拟，并通过外周注射非选择性肽CRF受体拮抗剂抑制。这种性质的发现是强大的证据表明，激活菌根中的外周CRF受体是肠道动力和粘膜功能的应力相关改变的重要机制。

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