Expression of cannabinoid CB1 receptors by vagal afferent neurons is inhibited by cholecystokinin
Expression of cannabinoid CB1 receptors by vagal afferent neurons is inhibited by cholecystokinin
复制标题
DOI：
10.1523/jneurosci.5404-03.2004
复制
发表时间：
2004-03-17
影响因子：
5.3
通讯作者：
Dockray, GJ
中科院分区：
文献类型：
--
作者：
Burdyga, G;Lal, S;Dockray, GJ
来自胃肠道的抑制性(饱腹感)和刺激性(食欲性)因素都调节食物的摄入量。在饱腹感荷尔蒙CCK的情况下，这些效应是通过迷走神经传入神经元介导的。我们现在报道，表达CCK-1受体的迷走神经传入神经元也表达大麻素CB1受体。逆行追踪证实这些神经元投射到胃和十二指肠。逆转录-聚合酶链式反应、免疫组织化学和原位杂交结果显示，停食12小时以上大鼠结状神经节中CB1受体的表达增加。免疫组织化学和原位杂交显示，禁食大鼠再喂养后，CB1受体的表达迅速丧失。这些作用可被CCK-1受体拮抗剂洛谷胺阻断，并被禁食大鼠的CCK所模拟。由于CCK是一种通过迷走神经起作用的饱腹感因子，而CB1激动剂刺激食物摄取，数据表明，一种新的机制调节来自胃肠道的饱腹感信号对食物摄入量的影响。
Both inhibitory ( satiety) and stimulatory (orexigenic) factors from the gastrointestinal tract regulate food intake. In the case of the satiety hormone cholecystokinin (CCK), these effects are mediated via vagal afferent neurons. We now report that vagal afferent neurons expressing the CCK-1 receptor also express cannabinoid CB1 receptors. Retrograde tracing established that these neurons project to the stomach and duodenum. The expression of CB1 receptors determined by RT-PCR, immunohistochemistry and in situ hybridization in rat nodose ganglia was increased by withdrawal of food for greater than or equal to12 hr. After refeeding of fasted rats there was a rapid loss of CB1 receptor expression identified by immunohistochemistry and in situ hybridization. These effects were blocked by administration of the CCK-1 receptor antagonist lorglumide and mimicked by administration of CCK to fasted rats. Because CCK is a satiety factor that acts via the vagus nerve and CB1 agonists stimulate food intake, the data suggest a new mechanism modulating the effect on food intake of satiety signals from the gastrointestinal tract.