Gamber Kevin M, Macarthur Heather, Westfall Thomas C
Department of Pharmacological and Physiological Science, Saint Louis University School of Medicine, 1402 South Grand Boulevard, Saint Louis, MO 63104, USA.
Neuropharmacology. 2005 Oct;49(5):646-52. doi: 10.1016/j.neuropharm.2005.04.017.
Little is known about the mechanism of action behind the orexigenic activity of cannabinoids. Neuropeptide Y (NPY) is one of the most potent orexigenic factors and is a key mediator in the hypothalamic control of food intake. We examined the effect of cannabinoids on NPY release using a rat hypothalamic explant model. The cannabinoid agonists anandamide (AEA) and CP55,940 both significantly augmented resting and KCl-evoked NPY release. AM251, a cannabinoid receptor antagonist, blocked the augmentation of NPY release elicited by AEA and CP55,940. Additionally, AM251 administered alone, in the absence of exogenous cannabinoid agonists, inhibited NPY release demonstrating the role of endogenous cannabinoids in NPY release. Combined, these findings demonstrate that cannabinoids augment NPY release in the hypothalamus and that this may be a potential mechanism behind the orexigenic activity of cannabinoids.
关于大麻素促食欲活性背后的作用机制，人们所知甚少。神经肽Y（NPY）是最有效的促食欲因子之一，是下丘脑控制食物摄入的关键介质。我们使用大鼠下丘脑外植体模型研究了大麻素对NPY释放的影响。大麻素激动剂花生四烯乙醇胺（AEA）和CP55,940均显著增加了静息状态下和氯化钾诱发的NPY释放。大麻素受体拮抗剂AM251可阻断AEA和CP55,940引起的NPY释放增加。此外，在没有外源性大麻素激动剂的情况下单独给予AM251可抑制NPY释放，这表明内源性大麻素在NPY释放中起作用。综合来看，这些发现表明大麻素可增加下丘脑NPY的释放，这可能是大麻素促食欲活性背后的潜在机制。
Zotero 插件