美国哥伦比亚大学Alexander R. Nectow课题组发现，脑干神经肽能神经元连接神经体液轴至饱足感。相关论文于2025年2月5日在线发表在《细胞》杂志上。

研究人员使用空间分辨的单细胞表型分析，描述了脑干中缝背核（DRN）中的一群神经肽能神经元，并阐述了它们如何调节饱足感。这些神经元从食物的感官呈现到摄入过程中追踪食物，将这些信号与较慢作用的体液信号整合，并表达胆囊收缩素（CCK）。

这些CCK神经元双向调节餐量，驱动一个具有内置延迟的持续餐终止信号。它们还处于感知和响应摄入的理想位置：其表达多种代谢信号因子，并整合到一个已知调节进食的扩展网络中。

总之，这项工作展示了DRN CCK神经元如何调节饱足感，并确定了一个可能的保守细胞机制，将多种神经体液信号转化为关键的行为输出。

据介绍，饥饿在演化中被连接，以确保动物有足够的能量生存和繁殖。知道何时开始进食与知道何时停止进食同样重要。

附：英文原文

Title: Brainstem neuropeptidergic neurons link a neurohumoral axis to satiation

Author: Srikanta Chowdhury, Nachiket G. Kamatkar, Wendy Xueyi Wang, Christa A. Akerele, Jiahao Huang, Junlin Wu, Amajindi Nwankpa, Charlotte M. Kane, Varun M. Bhave, Hao Huang, Xiao Wang, Alexander R. Nectow

Issue&Volume: 2025-02-05

Abstract: Hunger is evolutionarily hardwired to ensure that an animal has sufficient energy to survive and reproduce. Just as important as knowing when to start eating is knowing when to stop eating. Here, using spatially resolved single-cell phenotyping, we characterize a population of neuropeptidergic neurons in the brainstem’s dorsal raphe nucleus (DRN) and describe how they regulate satiation. These neurons track food from sensory presentation through ingestion, integrate these signals with slower-acting humoral cues, and express cholecystokinin (CCK). These CCK neurons bidirectionally regulate meal size, driving a sustained meal termination signal with a built-in delay. They are also well positioned to sense and respond to ingestion: they express a host of metabolic signaling factors and are integrated into an extended network known to regulate feeding. Together, this work demonstrates how DRN CCK neurons regulate satiation and identifies a likely conserved cellular mechanism that transforms diverse neurohumoral signals into a key behavioral output.

DOI: 10.1016/j.cell.2025.01.018

Source: https://www.cell.com/cell/abstract/S0092-8674(25)00047-9