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首页> 外文期刊>Neuron >Enhanced AMPA Receptor Trafficking Mediates the Anorexigenic Effect of Endogenous Glucagon-like Peptide-1 in the Paraventricular Hypothalamus
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Enhanced AMPA Receptor Trafficking Mediates the Anorexigenic Effect of Endogenous Glucagon-like Peptide-1 in the Paraventricular Hypothalamus

机译：增强的AMPA受体贩运介导内源性胰高血糖素样肽-1在椎间盘内下丘脑中的厌恶作用

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Summary Glucagon-like Peptide 1 (GLP-1)-expressing neurons in the hindbrain send robust projections to the paraventricular nucleus of the hypothalamus (PVN), which is involved in the regulation of food intake. Here, we describe that stimulation of GLP-1 afferent fibers within the PVN is sufficient to suppress food intake independent of glutamate release. We also show that GLP-1 receptor (GLP-1R) activation augments excitatory synaptic strength in PVN corticotropin-releasing hormone (CRH) neurons, with GLP-1R activation promoting a protein kinase A (PKA)-dependent signaling cascade leading to phosphorylation of serine S845 on GluA1 AMPA receptors and their trafficking to the plasma membrane. Finally, we show that postnatal depletion of GLP-1R in the PVN increases food intake and causes obesity. This study provides a comprehensive multi-level (circuit, synaptic, and molecular) explanation of how food intake behavior and body weight are regulated by endogenous central GLP-1. Video Abstract Display Omitted Highlights ? NTS-to-PVN projecting GLP-1 signaling suppresses food intake ? GLP-1 augments the excitatory synaptic strengths of CRH neurons via PKA pathway ? GLP-1 signaling in PVN causes phosphorylation of S845 of GluA1 Liu et?al. show that GLP-1 signaling in PVN suppresses food intake and may prevent obesity. The molecular mechanism underlying the GLP-1 function in the PVN is via AMPA receptor subunit-GluA1 phosphorylation and subsequent membrane trafficking in a PKA-dependent pathway.
机译：发明内容胰高血糖素样肽1（GLP-1） - 在后脑中的内部神经元送到下丘脑（PVN）的椎间盘（PVN）中的鲁棒突起，其参与食物摄入量。这里，我们描述了PVN内的GLP-1传入纤维的刺激足以抑制与谷氨酸释放相比的食物摄入量。我们还表明，GLP-1受体（GLP-1R）激活增强了PVN皮质甾醇释放激素（CRH）神经元的兴奋性突触强度，促进促进蛋白激酶A（PKA）依赖性信号级联导致磷酸化的蛋白激活对Glua1 AMPA受体的丝氨酸S845及其贩运血浆膜。最后，我们表明PVN中GLP-1R的产后消耗增加了食物摄入并导致肥胖。本研究提供了一种综合的多级（电路，突触和分子）解释食物摄入行为和体重是如何通过内源性中央GLP-1调节的。视频摘要显示省略了亮点吗？ NTS-to-PVN投影GLP-1信号抑制食物摄入量吗？ GLP-1通过PKA途径增强CRH神经元的兴奋性突触强度？ PVN中的GLP-1信号传导导致GLUA1 Liu Et的S845磷酸化。显示PVN中的GLP-1信号传导抑制食物摄入，可以防止肥胖。 PVN中GLP-1功能下面的分子机制是通过AMPA受体亚单次GLUA1磷酸化和随后在PKA依赖性途径中运输的膜。

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