Regulation of feeding by somatostatin neurons in the tuberal nucleus
Regulation of feeding by somatostatin neurons in the tuberal nucleus
复制标题
结节核中生长抑素神经元对进食的调节
DOI：
10.1126/science.aar4983
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发表时间：
2018-07-06
期刊：
影响因子：
56.9
通讯作者：
Fu, Yu
中科院分区：
文献类型：
--
作者：
Luo, Sarah Xinwei;Huang, Ju;Fu, Yu
调节进食的神经元结节核，下丘脑的一个区域，还没有被详细研究。Luo等人发现结节核中的GABA能生长抑素神经元在功能上参与调节小鼠的摄食（GABA，γ-氨基丁酸）（参见Diano的观点）。这些神经元被食物剥夺或饥饿激素激活。功能丧失和获得的实验表明，这些细胞是必要的，足以控制全身代谢平衡。这个新描述的调节中心通过投射到其他下丘脑核团与其他摄食控制回路广泛连接。在下丘脑的一个区域中，一组明确定义的神经元在控制进食中起着核心作用。结节核（TN）是一个令人惊讶的研究不足的大脑区域。我们发现，生长抑素（SST）神经元在TN，这是已知的人类神经退行性疾病中表现出病理或细胞学变化，在调节小鼠摄食起着至关重要的作用。GABA能结节SST（TNSST）神经元被饥饿和饥饿激素ghrelin激活。TNSST神经元的激活促进进食，而抑制减少它通过投射到室旁核和床核的终纹。TNSST神经元的消融减少了体重增加和食物摄入。这些发现揭示了一种以前未知的摄食调节机制，该机制通过食欲TNSST神经元起作用，为理解食欲变化提供了新的视角。
Neurons that regulate feeding The tuberal nucleus, an area of the hypothalamus, has not been studied in great detail. Luo et al. found that GABAergic somatostatin neurons in the tuberal nucleus are functionally involved in the regulation of feeding in mice (GABA, γ-aminobutyric acid) (see the Perspective by Diano). These neurons were activated by food deprivation or hunger hormone. Loss- and gain-of-function experiments indicated that these cells are necessary and sufficient to control systemic metabolic balance. This newly described regulatory center is extensively connected with other feeding control circuits via projections to other hypothalamic nuclei. Science, this issue p. 76; see also p. 29 A clearly defined group of neurons in an area of the hypothalamus plays a central role in the control of feeding. The tuberal nucleus (TN) is a surprisingly understudied brain region. We found that somatostatin (SST) neurons in the TN, which is known to exhibit pathological or cytological changes in human neurodegenerative diseases, play a crucial role in regulating feeding in mice. GABAergic tuberal SST (TNSST) neurons were activated by hunger and by the hunger hormone, ghrelin. Activation of TNSST neurons promoted feeding, whereas inhibition reduced it via projections to the paraventricular nucleus and bed nucleus of the stria terminalis. Ablation of TNSST neurons reduced body weight gain and food intake. These findings reveal a previously unknown mechanism of feeding regulation that operates through orexigenic TNSST neurons, providing a new perspective for understanding appetite changes.