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Nature:大麻素对进食的复杂效应

摘要 : 以前的研究工作确定了下丘脑 “阿黑皮素原”(POMC)神经元在因饱感而减少进食方面所起作用,说明促进进食的信号可能会降低POMC神经活性。Tamas Horvath及同事对这一观点进行了验证,发现令人意外的是,大麻素进食信号会增强POMC神经活性。这种矛盾的POMC神经激发作用对于在饱感状态由 “大麻素受体-1”的激活所触发的对进食的应有促进来说是必不可少的。

 以前的研究工作确定了下丘脑 “阿黑皮素原”(POMC)神经元在因饱感而减少进食方面所起作用,说明促进进食的信号可能会降低POMC神经活性。Tamas Horvath及同事对这一观点进行了验证,发现令人意外的是,大麻素进食信号会增强POMC神经活性。这种矛盾的POMC神经激发作用对于在饱感状态由 “大麻素受体-1”的激活所触发的对进食的应有促进来说是必不可少的。

作者得出结论认为,大麻素对进食的总体效应可能是由突触前和突触后两种效应驱动的(这两种效应彼此还可能是独立的),而造成总体行为变化的是它们在时间上的同步。

原文链接:Hypothalamic POMC neurons promote cannabinoid-induced feeding

Hypothalamic pro-opiomelanocortin (POMC) neurons promote satiety. Cannabinoid receptor 1 (CB1R) is critical for the central regulation of food intake. Here we test whether CB1R-controlled feeding in sated mice is paralleled by decreased activity of POMC neurons. We show that chemical promotion of CB1R activity increases feeding, and notably, CB1R activation also promotes neuronal activity of POMC cells. This paradoxical increase in POMC activity was crucial for CB1R-induced feeding, because designer-receptors-exclusively-activated-by-designer-drugs (DREADD)-mediated inhibition of POMC neurons diminishes, wheras DREADD-mediated activation of POMC neurons enhances CB1R-driven feeding. The Pomc gene encodes both the anorexigenic peptide α-melanocyte-stimulating hormone, and the opioid peptide β-endorphin. CB1R activation selectively increases β-endorphin but not α-melanocyte-stimulating hormone release in the hypothalamus, and systemic or hypothalamic administration of the opioid receptor antagonist naloxone blocks acute CB1R-induced feeding. These processes involve mitochondrial adaptations that, when blocked, abolish CB1R-induced cellular responses and feeding. Together, these results uncover a previously unsuspected role of POMC neurons in the promotion of feeding by cannabinoids.

对应Nature杂志: 2015年3月5日Nature杂志精选

来源: Nature 浏览次数:69

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