脑干 ADCYAP1 +神经元控制疾病行为的多个方面。感染会引起动物的一系列多效反应，包括厌食、倦怠、嗜睡和温度变化，统称为疾病行为。这些反应已被证明是适应性的。细菌内毒素（脂多糖 (LPS)）ー脑孤束核 (NTS) 和后区。节省代谢耗能，将能量留给免疫应答，对于个体的生存至关重要。本文是感染病等关联基础医学研究论文。
(Baidu Translation: )
When I was ill, I was trying to save my life. Nature reveals how the brain controls all these things. The brain controls energy conservation and immunity
Brain stem ADCYAP1+neurons control many aspects of disease behavior. Infection will cause a series of multi effect reactions of animals, including anorexia, fatigue, lethargy and temperature changes, which are collectively referred to as disease behaviors. These reactions have proved to be adaptive. Bacterial endotoxin (lipopolysaccharide (LPS)) affects the nucleus tractus solitarius (NTS) and the posterior region of the brain. Saving metabolic energy consumption and reserving energy for immune response is crucial for individual survival. This is a research paper on infectious diseases and other related basic medicine.
（百度翻訳： ）
病気になった時に「ならず者」になるのは命を守るためで、《自然》は脳がどのようにこれらのすべての脳を操作して省エネ免疫を操作するかを明らかにした
脳幹ADCYAP 1+ニューロンが疾病行為を制御する多方面。感染は動物の一連の多効果反応を引き起こし、拒食、倦怠、嗜眠と温度変化を含み、総称して疾病行為と呼ばれる。これらの反応は適応性であることが証明されている。細菌内毒素（リポ多糖（LPS））ー脳孤束核（NTS）と後部領域。代謝消費エネルギーを節約し、免疫応答にエネルギーを残すことは、個体の生存にとって極めて重要である。本文は感染症などの関連基礎医学研究論文である。
学术经纬
2022/11/02
论文
论文标题：Brainstem ADCYAP1+ neurons control multiple aspects of sickness behaviour
作者：Anoj Ilanges, Rani Shiao, Jordan Shaked, Ji-Dung Luo, Xiaofei Yu & Jeffrey M. Friedman
期刊：Nature
发表时间：2022/09/07
数字识别码：10.1038/s41586-022-05161-7
摘要：Infections induce a set of pleiotropic responses in animals, including anorexia, adipsia, lethargy and changes in temperature, collectively termed sickness behaviours1. Although these responses have been shown to be adaptive, the underlying neural mechanisms have not been elucidated2,3,4. Here we use of a set of unbiased methodologies to show that a specific subpopulation of neurons in the brainstem can control the diverse responses to a bacterial endotoxin (lipopolysaccharide (LPS)) that potently induces sickness behaviour. Whole-brain activity mapping revealed that subsets of neurons in the nucleus of the solitary tract (NTS) and the area postrema (AP) acutely express FOS after LPS treatment, and we found that subsequent reactivation of these specific neurons in FOS2A-iCreERT2 (also known as TRAP2) mice replicates the behavioural and thermal component of sickness. In addition, inhibition of LPS-activated neurons diminished all of the behavioural responses to LPS. Single-nucleus RNA sequencing of the NTS–AP was used to identify LPS-activated neural populations, and we found that activation of ADCYAP1+ neurons in the NTS–AP fully recapitulates the responses elicited by LPS. Furthermore, inhibition of these neurons significantly diminished the anorexia, adipsia and locomotor cessation seen after LPS injection. Together these studies map the pleiotropic effects of LPS to a neural population that is both necessary and sufficient for canonical elements of the sickness response, thus establishing a critical link between the brain and the response to infection.
