The central nervous system controls food consumption to maintain metabolic homoeostasis. In response to a meal, visceral signals from the gut activate neurons in the nucleus of the solitary tract (NTS) via the vagus nerve. These NTS neurons then excite brain regions known to mediate feeding behaviour, such as the lateral parabrachial nucleus (PBN). We previously described a neural circuit for appetite suppression involving calcitonin gene-related protein (CGRP)-expressing PBN (CGRP(PBN)) neurons; however, the molecular identity of the inputs to these neurons was not established. Here we identify cholecystokinin (CCK) and noradrenergic, dopamine β-hydroxylase (DBH)-expressing NTS neurons as two separate populations that directly excite CGRP(PBN) neurons. When these NTS neurons are activated using optogenetic or chemogenetic methods, food intake decreases and with chronic stimulation mice lose body weight. Our optogenetic results reveal that CCK and DBH neurons in the NTS directly engage CGRP(PBN) neurons to promote anorexia.

中文翻译：

---

从遗传和功能上讲，NTS是介导厌食症的PBN脑回路。

中枢神经系统控制食物消耗以维持代谢稳态。响应一顿饭，来自内脏的内脏信号会通过迷走神经激活孤立道（NTS）核中的神经元。然后，这些NTS神经元会激发已知的介导进食行为的大脑区域，例如臂外侧臂旁核（PBN）。先前我们描述了一种用于抑制食欲的神经回路，其中涉及表达降钙素基因相关蛋白（CGRP）的PBN（CGRP（PBN））神经元。但是，尚未确定这些神经元输入的分子身份。在这里，我们将胆囊收缩素（CCK）和去甲肾上腺素，多巴胺β-羟化酶（DBH）表达的NTS神经元确定为直接激发CGRP（PBN）神经元的两个单独的群体。当使用光遗传学或化学遗传学方法激活这些NTS神经元时，食物摄入减少，并且在长期刺激下小鼠体重减轻。我们的光遗传学结果显示NTS中的CCK和DBH神经元直接参与CGRP（PBN）神经元以促进厌食。