Cholecystokinin regulates expression of Y2 receptors in vagal afferent neurons serving the stomach.
Cholecystokinin regulates expression of Y2 receptors in vagal afferent neurons serving the stomach.
复制标题
胆囊动蛋白调节在为胃提供的迷走神经元中Y2受体的表达。
DOI：
10.1523/jneurosci.2493-08.2008
复制
发表时间：
2008-11-05
期刊：
影响因子：
--
通讯作者：
Dockray GJ
中科院分区：
文献类型：
--
作者：
Burdyga G;de Lartigue G;Raybould HE;Morris R;Dimaline R;Varro A;Thompson DG;Dockray GJ
肠激素CCK和PYY 3 -36通过迷走神经传入神经元抑制胃排空和食物摄取。在这里，我们报告说，CCK调节Y2 R的表达，PYY 3 -36的行为。在结状神经节大鼠禁食48小时，有一个5倍的减少Y2 R的mRNA相比，大鼠随意喂食;在禁食大鼠Y2 R的mRNA增加CCK的管理，并通过再喂养的机制敏感的CCK 1 R拮抗剂lorglumide。抗Y2 R抗体显示在神经元和卫星细胞中均有表达;前者大多数（89 ± 4%）也表达CCK 1 R。与禁食有损失的Y2 R免疫反应性CCK 1 R表达的神经元，其中许多投射到胃，但不是在卫星细胞或神经元投射到回肠或近端结肠。在培养的迷走神经传入神经元中，CCK和佛波酯分别使Y2 R启动子-荧光素酶报告基因（Y2 R-luc）的表达增加12.3±0.1倍和16.2±0.4倍;蛋白激酶C抑制剂Ro-32，0432可消除对两者的反应。PYY 3 -36刺激CREB磷酸化大鼠结状神经元后，引发CCK，在野生型小鼠PYY 3 -36增加Fos标记的脑干神经元，但在小鼠空CCK 1 R这种反应被取消。因此，Y2 R由投射到胃和回肠/结肠的结状神经节神经元的功能不同的子集表达;在前者中，表达依赖于CCK的刺激，并且有证据表明PYY 3 -36对迷走神经传入神经元的作用是CCK依赖性的。
The intestinal hormones CCK and PYY3-36 inhibit gastric emptying and food intake via vagal afferent neurons. Here we report that CCK regulates the expression of Y2R, at which PYY3-36 acts. In nodose ganglia from rats fasted up to 48h, there was a five-fold decrease of Y2R mRNA compared with rats fed ad libitum; Y2R mRNA in fasted rats was increased by administration of CCK, and by re-feeding through a mechanism sensitive to the CCK1R antagonist lorglumide. Antibodies to Y2R revealed expression in both neurons and satellite cells; most of the former (89 ± 4 %) also expressed CCK1R. With fasting there was loss of Y2R immunoreactivity in CCK1R expressing neurons many of which projected to the stomach, but not in satellite cells or neurons projecting to the ileum or proximal colon. Expression of a Y2R promoter-luciferase reporter (Y2R-luc) in cultured vagal afferent neurons was increased in response to CCK by 12.3±0.1-fold and by phorbol ester (16.2±0.4 fold); the response to both was abolished by the protein kinase C inhibitor Ro-32,0432. PYY3-36 stimulated CREB phosphorylation in rat nodose neurons after priming with CCK; in wild type mice PYY3-36 increased Fos labelling in brain stem neurons but in mice null for CCK1R this response was abolished. Thus Y2R is expressed by functionally distinct subsets of nodose ganglion neurons projecting to the stomach and ileum/colon; in the former expression is dependent on stimulation by CCK and there is evidence that PYY3-36 effects on vagal afferent neurons are CCK dependent.