Neuropeptide Y Suppresses Anorexigenic Output from the Ventromedial Nucleus of the Hypothalamus
Neuropeptide Y Suppresses Anorexigenic Output from the Ventromedial Nucleus of the Hypothalamus
复制标题
DOI：
10.1523/jneurosci.4031-09.2010
复制
发表时间：
2010-03-03
影响因子：
5.3
通讯作者：
Colmers, William F.
中科院分区：
文献类型：
--
作者：
Chee, Melissa J. S.;Myers, Martin G., Jr.;Colmers, William F.
下丘脑腹内侧核(VMN)的输出是厌食性的，并由瘦素的兴奋作用支持。VMN对神经肽Y(NPY)的促食欲作用也高度敏感。我们报道，NPY通过使VMN神经元超极化并降低其放电动作电位的能力来强烈地抑制VMN神经元。这一作用是通过Y-1受体激活GIRKs(G蛋白偶联的内向整流钾通道)来实现的。大约80%表达瘦素受体的VMN神经元对NPY的作用敏感，而VMN中75%的NPY敏感神经元对葡萄糖的反应是被葡萄糖升高统一抑制的。有趣的是，只有与36%的NPY敏感神经元相似，表达瘦素受体b的神经元也是葡萄糖敏感的。我们认为NPY可抑制瘦素兴奋的VMN神经元，从而阻止VMN神经元的厌食反应。这些结果进一步表明，VMN内厌食性和厌食性神经调节剂之间的动态相互作用直接影响能量平衡。
Output from the hypothalamic ventromedial nucleus (VMN) is anorexigenic and is supported by the excitatory actions of leptin. The VMN is also highly sensitive to the orexigenic actions of Neuropeptide Y (NPY). We report that NPY robustly inhibits VMN neurons by hyperpolarizing them and decreasing their ability to fire action potentials. This action was mediated by Y-1 receptors coupled to the activation of GIRKs (G-protein-coupled inwardly rectifying potassium channels). Approximately 80% of VMN neurons expressing leptin receptors were sensitive to the actions of NPY, whereas 75% of NPY-sensitive neurons in VMN also responded to glucose by being uniformly inhibited by elevations in glucose. Interestingly, only similar to 36% of NPY-sensitive, leptin receptor b-expressing neurons were also glucosensitive. We suggest that NPY inhibits VMN neurons that are excited by leptin, thereby arresting the anorexigenic tone exerted by VMN neurons. The results further suggest a dynamic interplay between anorexigenic and orexigenic neuromodulators within the VMN to directly affect energy balance.