Authors
Xinsong Guo, Mengyan Liu, Qingcheng Xiong, Howai Ngai, Mingdong He, Xinying Li, Yingwei Zheng, Fuqiang Xu, Minghong Ma, Ruiqi Wu
Published in
Proceedings of the National Academy of Sciences of the United States of America. Volume 123. Issue 34. Pages e2603853123. Aug 25, 2026. Epub Aug 18, 2026.
Abstract
Slow nasal breathing alleviates negative moods, but the precise nose-to-limbic pathways and their causal contributions remain unclear. Here, we identify a pathway in mice from olfactory sensory neurons (OSNs) in the nasal cavity to mitral cells in the olfactory bulb (OB), then to parvalbumin-positive (PV+) long-projecting interneurons in the perirhinal cortex (PRC), and subsequently to glutamatergic neurons in the posterior basolateral amygdala (pBLA), through which nasal afferent activity bidirectionally regulates anxiety in a frequency-dependent manner. Low-frequency nasal airflow or optogenetic OSN stimulation induced anxiolysis and increased PRC high-gamma power by activating PV+ neurons, whereas high-frequency had opposite effects. Chemogenetic silencing of the OB→PRCPV pathway eliminated the frequency-dependent regulation of anxiety-like behaviors driven by OSN stimulation. Selective activation or inhibition of the identified circuit generated opposing behavioral effects (anxiolytic vs. anxiogenic, respectively), paralleling the results of low- and high-frequency OSN stimulations. Strikingly, a 2-wk low-frequency nasal airflow/optogenetic OSN stimulation regimen ameliorated anxiety-like behaviors and restored PRC high-gamma activity in an anxiety model. This study reveals a nose-brain axis bidirectionally modulating anxiety via nasal afferent frequency, providing potential interventional strategies and targets for anxiety disorders.
PMID:
42611993
Bibliographic data and abstract were imported from PubMed on 19 Aug 2026.
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