CCK ELICITS AND MODULATES VAGAL AFFERENT ACTIVITY ARISING FROM GASTRIC AND DUODENAL SITES
CCK ELICITS AND MODULATES VAGAL AFFERENT ACTIVITY ARISING FROM GASTRIC AND DUODENAL SITES
复制标题
DOI：
10.1111/j.1749-6632.1994.tb44058.x
复制
发表时间：
1994-01-01
期刊：
影响因子：
--
通讯作者：
MORAN, TH
中科院分区：
文献类型：
--
作者：
SCHWARTZ, GJ;MORAN, TH
我们已经开始识别和表征对CCK敏感的迷走神经传入纤维在大鼠上胃肠道的位置和反应谱。我们发现胃和十二指肠迷走神经传入纤维对CCK和腔内负荷有反应。CCK既增敏又放大了这些纤维对负荷的反应，但可能是通过不同的转导机制实现的。因此，由胃十二指肠负荷和内源性CCK释放引起的饮食相关信号可以在外周传入迷走神经水平上整合。这些发现与行为学结果一致，表明胃负荷和外源性CCK的组合在抑制食物摄入方面比单独出现任何刺激都更有效。我们发现胃和十二指肠迷走神经传入纤维都对CCK敏感，这表明与食物相关的CCK可能作用于一系列连接上胃肠道和中枢神经系统底物的外周神经部位，这些底物是控制食物摄入的基础。内源性CCK激活胃迷走神经传入的方式可能是肠源性CCK的内分泌作用。另外，在靠近CCK释放位点的十二指肠负荷敏感迷走神经传入神经的新发现为内源性CCK在饱腹感介导中的局部旁分泌作用提供了可能。
We have begun to identify and characterize the locations and response profiles of vagal afferent fibers sensitive to CCK in the rat upper gastrointestinal tract. We found gastric and duodenal vagal afferent fibers that respond to CCK and to intraluminal loads. CCK both sensitizes and amplifies the response to loads in these fibers but may do so through separate transduction mechanisms. Thus, meal-related signals arising from the presence of gastroduodenal loads and the release of endogenous CCK can be integrated at the level of the peripheral afferent vagus nerve. These findings are consistent with behavioral results, demonstrating that combinations of gastric loads and exogenous CCK are more effective in suppressing food intake than is either stimulus presented alone. Our findings that both gastric and duodenal vagal afferent fibers are sensitive to CCK suggest that meal-related CCK may act at a range of peripheral neural sites linking the upper gastrointestinal tract to the central nervous system substrates underlying the control of food intake. The mode of activation of gastric vagal afferent by endogenously released CCK may be an endocrine action of intestinally derived CCK. Alternatively, the novel finding of duodenal load-sensitive vagal afferents close to a site of CCK release provides a potential for local paracrine actions of endogenous CCK in the mediation of satiety.