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Genetic identification of a neural circuit that suppresses appetite

机译：抑制食欲的神经回路的遗传鉴定

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摘要

Appetite suppression occurs after a meal and in conditions when it is unfavourable to eat, such as during illness or exposure to toxins. A brain region proposed to play a role in appetite suppression is the parabrachial nucleus, a heterogeneous population of neurons surrounding the superior cerebellar peduncle in the brainstem. The parabrachial nucleus is thought to mediate the suppression of appetite induced by the anorectic hormones amylin and cholecystokinin, as well as by lithium chloride and lipopolysaccharide, compounds that mimic the effects of toxic foods and bacterial infections, respectively. Hyperactivity of the parabrachial nucleus is also thought to cause starvation after ablation of orexigenic agouti-related peptide neurons in adult mice. However, the identities of neurons in the parabrachial nucleus that regulate feeding are unknown, as are the functionally relevant downstream projections. Here we identify calcitonin gene-related peptide-expressing neurons in the outer external lateral subdivision of the parabrachial nucleus that project to the latero-capsular division of the central nucleus of the amygdala as forming a functionally important circuit for suppressing appetite. Using genetically encoded anatomical, optogenetic and pharmacogenetic tools, we demonstrate that activation of these neurons projecting to the central nucleus of the amygdala suppresses appetite. In contrast, inhibition of these neurons increases food intake in circumstances when mice do not normally eat and prevents starvation in adult mice whose agouti-related peptide neurons are ablated. Taken together, our data demonstrate that this neural circuit from the parabrachial nucleus to the central nucleus of the amygdala mediates appetite suppression in conditions when it is unfavourable to eat. This neural circuit may provide targets for therapeutic intervention to overcome or promote appetite.
机译：进餐后以及在不宜进食的情况下（例如在生病或接触毒素期间）会发生食欲抑制。拟在食欲抑制中发挥作用的大脑区域是臂旁旁核，这是围绕脑干上小脑梗的神经元的异质群体。认为臂旁旁核抑制食欲抑制作用，所述抑制作用是由厌食激素胰岛淀粉样多肽和胆囊收缩素以及氯化锂和脂多糖（分别模拟有毒食物和细菌感染的化合物）诱导的。还认为，成年小鼠食欲原性刺豚鼠相关肽神经元消融后，臂旁核的过度活动会引起饥饿。然而，调控进食的臂旁神经核中神经元的身份以及功能相关的下游预测都是未知的。在这里我们确定降钙素基因相关肽表达的神经元在臂旁旁核的外部外部横向细分中，这些神经元投射到杏仁核中央核的lateo-荚膜分裂，形成抑制食欲的重要功能电路。使用遗传编码的解剖学，光遗传学和药物遗传学工具，我们证明了这些神经元的激活投射到杏仁核的中央核抑制食欲。相反，在小鼠通常不进食的情况下，对这些神经元的抑制作用会增加食物摄入，并会消除与刺痛相关的肽神经元的成年小鼠饥饿。两者合计，我们的数据表明，从臂旁旁核到杏仁核中央核的这种神经回路在不宜进食的情况下会抑制食欲。该神经回路可以为治疗干预提供目标，以克服或促进食欲。

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  • 来源
    《Nature》 |2013年第7474期|111-114|共4页
  • 作者

    Matthew E. Carter; Marta E. Soden; Larry S. Zweifel; Richard D. Palmiter;

  • 作者单位

    Howard Hughes Medical Institute, University of Washington, Seattle, Washington 98195, USA,Department of Biochemistry, University of Washington, Seattle, Washington 98195, USA,Department of Biology, Williams College, Williamstown, Massachusetts 01267, USA;

    Department of Pharmacology, University of Washington, Seattle, Washington 98195, USA,Department of Psychiatry, University of Washington, Seattle, Washington 98195, USA;

    Department of Pharmacology, University of Washington, Seattle, Washington 98195, USA,Department of Psychiatry, University of Washington, Seattle, Washington 98195, USA;

    Howard Hughes Medical Institute, University of Washington, Seattle, Washington 98195, USA,Department of Biochemistry, University of Washington, Seattle, Washington 98195, USA;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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