河北医科大学袁芳课题组的一项最新研究开发出了孤束核中表达瘦素受体的神经元对通气稳态作用的环路机制。相关论文于2026年4月6日发表在《神经科学通报》杂志上。

在这项研究中，课题组研究人员确定了呼气量与呼气量的比值作为易感C57BL/6J小鼠呼气后呼吸暂停的潜在预测因子。该课题组证明，瘦素信号在核细胞孤立束（NTS）中是维持呼吸驱动和抑制呼吸暂停的关键。表达瘦素受体b的NTS （NTSLepRb）神经元的化学发生激活显著降低了呼吸暂停的发生率，而它们的消融加剧了呼吸功能障碍。

此外，NTSLepRb神经元通过解剖学上和功能上分离的投射到下丘脑背内侧和外侧臂旁核来介导这些效应。这些发现定义了一个特定的瘦素介导的脑干回路，稳定呼吸输出，为睡眠呼吸障碍提供了新的机制见解和潜在的治疗靶点。

据悉，睡眠呼吸暂停综合征（SAS）是一种常见的疾病，其特征是睡眠期间反复出现呼吸系统疾病；然而，控制呼吸稳定性的神经机制仍然知之甚少。

附：英文原文

Title: Circuit Mechanisms Underlying the Contribution of Leptin Receptor-Expressing Neurons in the Nucleus Tractus Solitarius to Ventilatory Homeostasis

Author: Hao, Yinchao, Zhu, Mengchu, Yu, Hongxiao, Zhang, Xiang, Shi, Yishuo, Sun, Lu, Hao, Yaxin, Huang, Yifei, Yu, Lingxiao, Wang, Sheng, Zhao, Dongxing, Yuan, Fang

Issue&Volume: 2026-04-06

Abstract: Sleep apnea syndrome (SAS) is a prevalent disorder characterized by recurrent respiratory pauses during sleep; however, the neural mechanisms governing respiratory stability remain poorly understood. In this study, we identify the ratio of sigh expiratory volume to eupneic expiratory volume as a potential predictor of post-sigh apnea in susceptible C57BL/6J mice. We demonstrate that leptin signaling within the nucleus tractus solitarius (NTS) is critical for maintaining respiratory drive and suppressing apnea. Chemogenetic activation of Leptin receptor b-expressing NTS (NTSLepRb) neurons significantly reduced apnea incidence, whereas their ablation exacerbated respiratory dysfunction. Moreover, NTSLepRb neurons mediate these effects through anatomically and functionally segregated projections to the dorsomedial hypothalamus and the lateral parabrachial nucleus. These findings define a specific leptin-mediated brainstem circuit that stabilizes respiratory output, providing new mechanistic insights and potential therapeutic targets for sleep-disordered breathing.

DOI: 10.1007/s12264-026-01614-5

Source: https://link.springer.com/article/10.1007/s12264-026-01614-5