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Abstract：
A fundamental question of physiology is how gut-brain signaling stimulates appetite. While many studies have emphasized the importance of vagal afferents to the brain in inducing satiation, little is known about whether and how the vagal-mediated gut-brain pathway senses orexigenic signals and stimulates feeding. Here, we identified a previously uncharacterized population of fasting-activated catecholaminergic neurons in the nucleus of the solitary tract (NTS). After characterizing the anatomical complexity among NTS catecholaminergic neurons, we surprisingly found that activation of NTS epinephrine (ENTS) neurons co-expressing neuropeptide Y (NPY) stimulated feeding, whereas activation of NTS norepinephrine (NENTS) neurons suppressed feeding. Monosynaptic tracing/activation experiments then showed that these NTS neurons receive direct vagal afferents from nodose neurons. Moreover, activation of the vagal→NPY/ENTS neural circuit stimulated feeding. Our study reveals an orexigenic role of the vagal→NTS pathway in controlling feeding, thereby providing important insights about how gut-brain signaling regulates feeding behavior.
摘要：
生理学的一个基本问题是肠-脑信号如何刺激食欲。虽然许多研究强调迷走神经传入大脑在诱导饱腹感方面的重要性，关于迷走神经介导的肠-脑通路是否以及如何感知食欲信号并刺激进食，人们知之甚少。这里,我们在孤束核(NTS)中发现了一个先前未被表征的禁食激活儿茶酚胺能神经元群体.在表征NTS儿茶酚胺能神经元的解剖复杂性后，我们惊讶地发现，NTS肾上腺素（ENTS）神经元共表达神经肽Y（NPY）刺激摄食，而NTS去甲肾上腺素（NENTS）神经元的激活抑制了摄食。然后，单突触追踪/激活实验表明，这些NTS神经元从结节神经元接收直接的迷走神经传入。此外，迷走神经激活→NPY/ENTS神经回路刺激进食。我们的研究揭示了迷走神经→NTS途径在控制摄食中的食欲作用，从而提供有关肠脑信号如何调节摄食行为的重要见解。
