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A hindbrain dopaminergic neural circuit prevents weight gain by reinforcing food satiation.后脑多巴胺能神经回路通过加强食物饱腹感来防止体重增加。
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Autosomal recessive complete STAT1 deficiency caused by compound heterozygous intronic mutations.常染色体隐性完全 STAT1 缺陷症由复合杂合内含子突变引起。
Int Immunol. 2020 Sep 30;32(10):663-671. doi: 10.1093/intimm/dxaa043.
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Pharmacotherapeutic strategies for the treatment of anorexia nervosa - too much for one drug?治疗神经性厌食症的药物治疗策略——一种药物是否太多？
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Dopamine D2 receptor overexpression in the nucleus accumbens core induces robust weight loss during scheduled fasting selectively in female mice.伏隔核核心区多巴胺D2受体过表达会在雌性小鼠定时禁食期间选择性地导致显著体重减轻。
Mol Psychiatry. 2021 Aug;26(8):3765-3777. doi: 10.1038/s41380-019-0633-8. Epub 2019 Dec 20.
7
A POMC-originated circuit regulates stress-induced hypophagia, depression, and anhedonia.一个源于 POMC 的回路调节应激引起的摄食量减少、抑郁和快感缺失。
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Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa.全基因组关联研究确定了 8 个风险位点，并提示神经性厌食症与代谢-精神起源有关。
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Rostral and Caudal Ventral Tegmental Area GABAergic Inputs to Different Dorsal Raphe Neurons Participate in Opioid Dependence.腹侧被盖区的头端和尾端 GABA 能传入不同的中缝背核神经元参与阿片类药物依赖。
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Exploration of Shared Genetic Architecture Between Subcortical Brain Volumes and Anorexia Nervosa.探讨皮质下脑体积与神经性厌食症之间的共享遗传结构。
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中脑 5-HT 神经元的多巴胺能传入从 D2 向 D1 转变会导致小鼠厌食。

A D2 to D1 shift in dopaminergic inputs to midbrain 5-HT neurons causes anorexia in mice.

机构信息

Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA.

Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, China.

出版信息

Nat Neurosci. 2022 May;25(5):646-658. doi: 10.1038/s41593-022-01062-0. Epub 2022 May 2.

DOI:10.1038/s41593-022-01062-0
PMID:35501380
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9926508/
Abstract

Midbrain dopamine (DA) and serotonin (5-HT) neurons regulate motivated behaviors, including feeding, but less is known about how these circuits may interact. In this study, we found that DA neurons in the mouse ventral tegmental area bidirectionally regulate the activity of 5-HT neurons in the dorsal raphe nucleus (DRN), with weaker stimulation causing DRD2-dependent inhibition and overeating, while stronger stimulation causing DRD1-dependent activation and anorexia. Furthermore, in the activity-based anorexia (ABA) paradigm, which is a mouse model mimicking some clinical features of human anorexia nervosa (AN), we observed a DRD2 to DRD1 shift of DA neurotransmission on 5-HT neurons, which causes constant activation of these neurons and contributes to AN-like behaviors. Finally, we found that systemic administration of a DRD1 antagonist can prevent anorexia and weight loss in ABA. Our results revealed regulation of feeding behavior by stimulation strength-dependent interactions between DA and 5-HT neurons, which may contribute to the pathophysiology of AN.

摘要

中脑多巴胺 (DA) 和 5-羟色胺 (5-HT) 神经元调节动机行为，包括进食，但对于这些回路如何相互作用知之甚少。在这项研究中，我们发现小鼠腹侧被盖区的 DA 神经元双向调节背侧中缝核 (DRN) 中 5-HT 神经元的活动，较弱的刺激导致 DRD2 依赖性抑制和暴食，而较强的刺激导致 DRD1 依赖性激活和厌食。此外，在活动性厌食 (ABA) 范式中，我们观察到 5-HT 神经元上的 DA 神经传递从 DRD2 向 DRD1 转变，这导致这些神经元持续激活，并有助于类似 AN 的行为。最后，我们发现系统给予 DRD1 拮抗剂可以预防 ABA 中的厌食和体重减轻。我们的结果揭示了 DA 和 5-HT 神经元之间刺激强度依赖性相互作用对进食行为的调节，这可能有助于 AN 的病理生理学。