Neural networks of several novel neuropeptides involved in feeding regulation.
Neural networks of several novel neuropeptides involved in feeding regulation.
复制标题
DOI：
10.1016/j.nut.2008.06.016
复制
发表时间：
2008-09
期刊：
影响因子：
4.4
通讯作者：
S. Shioda;F. Takenoya;M. Yagi;Lihua Wang;Yasunori Hori;H. Kageyama
中科院分区：
文献类型：
--
作者：
S. Shioda;F. Takenoya;M. Yagi;Lihua Wang;Yasunori Hori;H. Kageyama
新型神经肽作为G蛋白偶联受体（GPCR）的配体被定位于大脑中，并发挥一系列生理功能，其中之一是摄食调节。我们描述了这些最近发现的GPCR配体的分布和定位，并回顾了它们在神经网络中的参与，特别是在摄食调节中。本文综述了一些新型GPCR配体的研究进展，包括食欲素、生长激素释放肽、甘丙肽样肽等摄食调节神经肽以及神经肽Y、阿黑皮素原等已知神经肽。我们的研究小组和其他人已经研究了这些神经肽，特别是关于含有这些神经肽的神经元在下丘脑中的相互作用。在下丘脑中，这些神经元之间的串扰在决定进食状态和进食行为中起着关键作用。我们描述了这些神经肽的一些结构和功能特征，并总结了下丘脑中不同种类的摄食调节神经元和瘦素靶向神经元之间的已知相互作用。此外，我们提出了一种新的策略，用于分析神经回路，涉及这些喂养调节GPCR配体在大脑中，在这一领域的研究通过使用转基因小鼠模型的帮助。我们还介绍了我们最近的研究结果，涉及摄食调节，能量稳态和体温调节方面。这一领域的研究将在阐明食欲障碍和疾病的神经学原因方面发挥重要作用，并可能有助于为患有此类疾病的患者建立新的治疗方法。
Novel neuropeptides acting as G-protein–coupled receptor (GPCR) ligands are known to be localized in the brain and play a range of physiologic functions, one of which is feeding regulation. We describe the distribution and localization of these recently identified GPCR ligands and review their involvement in neuronal networks, particularly in feeding regulation. This review addresses aspects of some novel GPCR ligands, including feeding-regulating neuropeptides such as orexin, ghrelin, and galanin-like peptide and other known neuropeptides such as neuropeptide Y and pro-opiomelanocortin. These neuropeptides have been studied by our research group and others, particularly with regard to interactions in the hypothalamus of neurons containing these neuropeptides. In the hypothalamus, cross-talk among such neurons plays a key role in determining feeding states and feeding behavior. We describe some structural and functional characteristics of these neuropeptides and summarize the known interactions between the different kinds of feeding-regulating neurons and leptin-targeting neurons in the hypothalamus. Moreover, we present a new strategy for analyzing neural circuits involving these feeding-regulating GPCR ligands in the brain, with research in this field aided by the use of transgenic mouse models. We also present our recent results that involve aspects of feeding regulation, energy homeostasis, and body temperature regulation. Research in this field will serve the important role of clarifying neurologically based causes for appetite dysfunctions and diseases and may help in establishing new therapies for patients with such conditions.