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首页> 外文期刊>American Journal of Physiology >Postprandial neuronal activation in the nucleus of the solitary tract is partly mediated by CCK-A receptors.
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Postprandial neuronal activation in the nucleus of the solitary tract is partly mediated by CCK-A receptors.

机译：餐道神经元的餐后神经元活化部分地由CCK-A受体介导。

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CCK-A receptors and neurons of the nucleus of the solitary tract (NTS) are involved in the regulation of food intake, and in rats, there is evidence for involvement of an intestinal vagal afferent pathway. Studies investigating the role of CCK-A receptors in activation of NTS neurons using highly selective CCK-A receptor agonists and antagonists have yielded conflicting data. In the present study, we investigated CCK-induced and postprandial activation of NTS neurons, together with food intake studies, in CCK-A receptor-deficient Otsuka Long-Evans Tokushima fatty (OLETF) rats. Activated NTS neurons were detected using immunohistological staining for c-Fos protein. Exogenous CCK increased the number of c-Fos protein-positive cells in the NTS of Sprague-Dawley and CCK-A receptor-intact Long-Evans Tokushima Otsuka (LETO) rats but had no effect in CCK-A receptor-deficient OLETF rats. Food intake-induced c-Fos protein expression in NTS neurons was significantly reduced in CCK-A receptor-deficient OLETF ratscompared with Sprague-Dawley or LETO rats. Postprandial c-Fos protein expression in the NTS was also significantly decreased after pretreatment with the CCK-A receptor antagonist MK329 after both short- and long-term fasting periods. Exogenous CCK decreased cumulative food intake in Sprague-Dawley and LETO rats but not in OLETF rats. These data demonstrate that CCK-A receptors are involved in the CCK- and food-induced c-Fos protein expression in the NTS. Taken together with the results of the food intake studies, this suggests that activation of CCK-A receptors is involved in the postprandial activation of NTS neurons and in the regulation of food intake.
机译：CCK-A受体和孤立道核（NTS）的神经元参与食物摄入的调节，在大鼠中，有证据表明肠道迷走神经传入途径参与其中。使用高选择性CCK-A受体激动剂和拮抗剂研究CCK-A受体在NTS神经元激活中的作用的研究得出了相互矛盾的数据。在本研究中，我们调查了CCK-A受体缺陷型大冢长埃文斯德岛脂肪（OLETF）大鼠的CCK诱导和餐后NTS神经元活化。使用c-Fos蛋白的免疫组织学染色检测激活的NTS神经元。外源性CCK增加了Sprague-Dawley和CCK-A受体完整的长埃文斯德岛大冢（LETO）大鼠的NTS中c-Fos蛋白阳性细胞的数量，但对CCK-A受体缺陷型OLETF大鼠没有影响。与Sprague-Dawley或LETO大鼠相比，CCK-A受体缺陷型OLETF大鼠的NTS神经元中食物摄入诱导的c-Fos蛋白表达显着降低。在短期和长期禁食期后，用CCK-A受体拮抗剂MK329预处理后，NTS中的餐后c-Fos蛋白表达也显着降低。外源性CCK降低了Sprague-Dawley和LETO大鼠的累积食物摄入量，但没有降低OLETF大鼠的累积食物摄入量。这些数据表明，CCK-A受体参与了NTS中CCK和食物诱导的c-Fos蛋白表达。结合食物摄入研究的结果，这表明CCK-A受体的激活与NTS神经元的餐后激活以及食物摄入的调节有关。

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