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伏隔核中μ阿片受体激活诱导的高脂肪摄入被 Y1R 阻断和 MC3/4R 刺激所抑制。

High-fat intake induced by mu-opioid activation of the nucleus accumbens is inhibited by Y1R-blockade and MC3/4R- stimulation.

机构信息

Neurobiology of Nutrition Laboratory, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70808, USA.

出版信息

Brain Res. 2010 Sep 2;1350:131-8. doi: 10.1016/j.brainres.2010.03.061. Epub 2010 Mar 24.

Abstract

Nucleus accumbens mu-opioid receptor activation can strongly stimulate intake of high-fat food in satiated rats, and one of the mechanisms involves activation of lateral hypothalamic orexin neurons and orexin receptor-1 signaling in the mesolimbic dopamine system. Here, we tested the potential contribution of NPY/Y1R and alpha-MSH/MC3/4R-signaling to accumbens-induced high-fat feeding. Prior administration of the selective Y1R antagonist 1229U91 or the MC3/4R agonist MTII into the lateral ventricle (LV) dose-dependently decreased high-fat intake induced by nucleus accumbens injection of the mu-opioid receptor agonist DAMGO. Both drugs also decreased high-fat feeding induced by switching rats from regular chow to high-fat diet, but less efficiently than when DAMGO-induced. Administration of 1229U91 directly into the PVH also suppressed DAMGO-induced high-fat intake, but a higher dose was required. The results suggest that NPY/Y1R signaling in the PVH and other forebrain sites is necessary for accumbens DAMGO to elicit high-fat intake, and that forebrain MC3/4R signaling can suppress it.

摘要

伏隔核 μ 阿片受体的激活可以强烈刺激饱食大鼠摄入高脂肪食物,其机制之一涉及外侧下丘脑食欲素神经元的激活和中脑边缘多巴胺系统中食欲素受体-1 信号传导。在这里,我们测试了 NPY/Y1R 和 α-MSH/MC3/4R 信号传导对伏隔核诱导的高脂肪进食的潜在贡献。选择性 Y1R 拮抗剂 1229U91 或 MC3/4R 激动剂 MTII 预先给药到侧脑室(LV)可剂量依赖性地降低由伏隔核注射 μ 阿片受体激动剂 DAMGO 诱导的高脂肪摄入。这两种药物也降低了大鼠从常规饲料转换为高脂肪饮食时的高脂肪进食,但效果不如 DAMGO 诱导的那么好。1229U91 直接给药到 PVH 也抑制了 DAMGO 诱导的高脂肪摄入,但需要更高的剂量。结果表明,PVH 和其他前脑部位的 NPY/Y1R 信号传导对于伏隔核 DAMGO 引发高脂肪摄入是必要的,并且前脑 MC3/4R 信号传导可以抑制它。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3435/2926229/6b8eee812ffc/nihms199429f1.jpg

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