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NTS儿茶酚胺神经元介导低血糖饥饿
作者:小柯机器人 发布时间:2019/12/16 14:35:55

美国爱荷华大学Deniz Atasoy研究小组发现,NTS儿茶酚胺神经元通过下丘脑内侧进食途径介导低血糖饥饿。该研究于2019年12月12日在线发表于国际一流学术期刊《细胞—代谢》。

研究人员报道了从孤束核(NTS)表达酪氨酸羟化酶(TH)神经元的葡萄糖缺乏喂养途径,该神经元密集投射到下丘脑,并通过对刺鼠相关肽(AgRP)和丙型黑素皮质激素(POMC)表达的神经元的双向肾上腺素能调节来引起进食。弓形核(ARC)投射NTSTH神经元或它们的靶标AgRP神经元的急性化学生成抑制作用,削弱了2-脱氧-D-葡萄糖(2DG)注射引起的糖皮质激素进食。

神经解剖学追踪结果表明,投射ARC的食欲性NTSTH神经元与投射到可促进饱腹感的臂旁核(PBN)的邻儿茶酚胺神经元大不相同。

总的来说,研究人员描述了一个回路组织,其中来自脑干的上升途径可响应低血糖,通过下丘脑中的关键饥饿神经元刺激食欲。

据介绍,葡萄糖是大脑的重要能量来源,由能量缺乏或治疗药物引发的缺乏可能致命。食欲增加是抵抗低血糖的关键行为防御; 然而,所涉及的主要途径尚不清楚。

附:英文原文

Title: NTS Catecholamine Neurons Mediate Hypoglycemic Hunger via Medial Hypothalamic Feeding Pathways

Author: Iltan Aklan, Nilufer Sayar Atasoy, Yavuz Yavuz, Tayfun Ates, Ilknur Coban, Fulya Koksalar, Gizem Filiz, Iskalen Cansu Topcu, Merve Oncul, Pelin Dilsiz, Utku Cebecioglu, Muhammed Ikbal Alp, Bayram Yilmaz, Deborah R. Davis, Karolina Hajdukiewicz, Kenji Saito, Witold Konopka, Huxing Cui, Deniz Atasoy

Issue&Volume: December 12, 2019

Abstract: Glucose is the essential energy source for the brain, whose deficit, triggered byenergy deprivation or therapeutic agents, can be fatal. Increased appetite is thekey behavioral defense against hypoglycemia; however, the central pathways involvedare not well understood. Here, we describe a glucoprivic feeding pathway by tyrosinehydroxylase (TH)-expressing neurons from nucleus of solitary tract(NTS), which projectdensely to the hypothalamus and elicit feeding through bidirectional adrenergic modulationof agouti-related peptide (AgRP)- and proopiomelanocortin (POMC)-expressing neurons.Acute chemogenetic inhibition of arcuate nucleus (ARC)-projecting NTSTH neurons or their target, AgRP neurons, impaired glucoprivic feeding induced by 2-Deoxy-D-glucose(2DG) injection. Neuroanatomical tracing results suggested that ARC-projecting orexigenicNTSTH neurons are largely distinct from neighboring catecholamine neurons projecting toparabrachial nucleus (PBN) that promotes satiety. Collectively, we describe a circuitorganization in which an ascending pathway from brainstem stimulates appetite throughkey hunger neurons in the hypothalamus in response to hypoglycemia.

DOI: 10.1016/j.cmet.2019.11.016

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(19)30623-0

期刊信息

Cell Metabolism:《细胞—代谢》,创刊于2005年。隶属于细胞出版社,最新IF:22.415
官方网址:https://www.cell.com/cell-metabolism/home
投稿链接:https://www.editorialmanager.com/cell-metabolism/default.aspx