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首页> 外文期刊>Cell metabolism >NTS Catecholamine Neurons Mediate Hypoglycemic Hunger via Medial Hypothalamic Feeding Pathways
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NTS Catecholamine Neurons Mediate Hypoglycemic Hunger via Medial Hypothalamic Feeding Pathways

机译：NTS Catecholamine神经元通过内侧下丘脑喂养途径调解降血糖饥饿

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摘要

Glucose is the essential energy source for the brain, whose deficit, triggered by energy deprivation or therapeutic agents, can be fatal. Increased appetite is the key behavioral defense against hypoglycemia; however, the central pathways involved are not well understood. Here, we describe a glucoprivic feeding pathway by tyrosine hydroxylase (TH)-expressing neurons from nucleus of solitary tract (NTS), which project densely to the hypothalamus and elicit feeding through bidirectional adrenergic modulation of 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 orexigenic NTSTH neurons are largely distinct from neighboring catecholamine neurons projecting to parabrachial nucleus (PBN) that promotes satiety. Collectively, we describe a circuit organization in which an ascending pathway from brainstem stimulates appetite through key hunger neurons in the hypothalamus in response to hypoglycemia.
机译：葡萄糖是大脑的基本能源，其缺陷，由能量剥夺或治疗剂引发，可能是致命的。增加的食欲是对低血糖症的关键行为防御;然而，所涉及的中央途径尚不清楚。在这里，我们描述了酪氨酸羟基化酶（Th）-Exexing的神经元（NTS）的葡萄糖喂养途径，其致密地将丘脑和通过双向肾上腺素能调制引发饲料，这些抗蛋白酶有关的蛋白质（AGRP） - 和Proopioomelanocortin （POMC） - 抑制神经元。弓形核（ARC）的急性化学抑制 - 重新喷射NTSTH神经元或其靶，AGRP神经元，由2-脱氧-D-葡萄糖（2DG）注射诱导的葡萄糖喂养受损。神经杀菌追踪结果表明，突出的丙烯酸NTSTH神经元在很大程度上不同于突出促进饱腹腹筋细胞核（PBN）的相邻的儿茶酚胺神经元。统称，我们描述了一种电路组织，其中来自脑干的上升途径通过下丘脑中的次核饥饿神经元刺激食欲，以应对低血糖。

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