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本文引用的文献

1
GABAergic signaling by AgRP neurons prevents anorexia via a melanocortin-independent mechanism.AgRP 神经元的 GABA 能信号通过一种独立于黑皮质素的机制来防止厌食症。
Eur J Pharmacol. 2011 Jun 11;660(1):21-7. doi: 10.1016/j.ejphar.2010.10.110. Epub 2011 Jan 3.
2
Modulation of the central melanocortin system by leptin, insulin, and serotonin: co-ordinated actions in a dispersed neuronal network.瘦素、胰岛素和血清素对中枢黑色素皮质系统的调制：分散神经元网络中的协同作用。
Eur J Pharmacol. 2011 Jun 11;660(1):2-12. doi: 10.1016/j.ejphar.2010.11.042. Epub 2011 Jan 3.
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AGRP neurons are sufficient to orchestrate feeding behavior rapidly and without training.AGRP 神经元足以快速协调进食行为，而无需进行训练。
Nat Neurosci. 2011 Mar;14(3):351-5. doi: 10.1038/nn.2739. Epub 2010 Jan 5.
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Mechanism of the development of obesity in animals with hypothalamic lesions.下丘脑损伤动物肥胖发生的机制。
Physiol Rev. 1946 Oct;26(4):541-59. doi: 10.1152/physrev.1946.26.4.541.
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Regulation of parkinsonian motor behaviours by optogenetic control of basal ganglia circuitry.通过光遗传学控制基底神经节回路调节帕金森运动行为。
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Synaptic release of GABA by AgRP neurons is required for normal regulation of energy balance.AgRP神经元突触释放γ-氨基丁酸（GABA）是能量平衡正常调节所必需的。
Nat Neurosci. 2008 Sep;11(9):998-1000. doi: 10.1038/nn.2167.
7
Agouti-related peptide-expressing neurons are mandatory for feeding.表达刺鼠相关肽的神经元对进食至关重要。
Nat Neurosci. 2005 Oct;8(10):1289-91. doi: 10.1038/nn1548. Epub 2005 Sep 11.
8
Millisecond-timescale, genetically targeted optical control of neural activity.神经活动的毫秒级、基因靶向光学控制。
Nat Neurosci. 2005 Sep;8(9):1263-8. doi: 10.1038/nn1525. Epub 2005 Aug 14.
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Diabetes, obesity, and the brain.糖尿病、肥胖与大脑。
Science. 2005 Jan 21;307(5708):375-9. doi: 10.1126/science.1104344.
10
Transgenic neuronal expression of proopiomelanocortin attenuates hyperphagic response to fasting and reverses metabolic impairments in leptin-deficient obese mice.阿片促黑皮质素原的转基因神经元表达减弱了瘦素缺乏型肥胖小鼠对禁食的贪食反应，并逆转了代谢障碍。
Diabetes. 2003 Nov;52(11):2675-83. doi: 10.2337/diabetes.52.11.2675.

点亮下丘脑：摄食行为的协调控制。

Lighting up the hypothalamus: coordinated control of feeding behavior.

出版信息

Nat Neurosci. 2011 Mar;14(3):277-8. doi: 10.1038/nn0311-277.

DOI:10.1038/nn0311-277
PMID:21346745
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3755601/
Abstract

A new optogenetics study finds that stimulation of pro-opiomelanocortin (POMC) and agouti-related peptide (AGRP) neurons acutely regulates feeding behavior. AGRP-induced hyperphagia is independent of melanocortin signaling.

摘要

一项新的光遗传学研究发现，促阿黑皮素原（POMC）和刺鼠相关肽（AGRP）神经元的刺激可急性调节摄食行为。AGRP 诱导的多食症不依赖于黑素皮质素信号。