Scientists identify the nose-to-brain circuit that makes slow breathing calming
New research shows that slow nasal breathing directly reduces anxiety by activating a specific nose-to-brain circuit, while fast breathing worsens it. The findings, published in PNAS, suggest the physical rhythm of airflow acts as an emotional dial.
Scientists have discovered a specific circuit in the brain that connects the nose to emotion centers, which can reduce anxiety when we breathe slowly through our noses. Fast breathing appears to have the opposite effect. Researchers from Fudan University in China published their findings in the Proceedings of the National Academy of Sciences (PNAS).
The team investigated how different breathing frequencies affect anxiety in mice. They measured the natural breathing rates of mice and created three categories: slow (two breaths per second), moderate (four breaths per second), and fast (seven breaths per second) breathing frequencies. Using optogenetics, they controlled the activity of olfactory sensory neurons in the mice's nasal cavities by shining a blue laser through fiber optic cables.
During the experiments, the mice were placed in behavioral arenas designed to assess their anxiety levels. In the Elevated Plus Maze and Open Field Test, mice naturally avoid open spaces, which indicates lower anxiety. When the researchers stimulated the nasal neurons at a slow rate, the mice spent more time in the open areas, suggesting a calmer state. Conversely, fast stimulation increased anxiety.
To understand what was happening in the brain, the researchers recorded electrical activity in the perirhinal cortex, an area associated with memory and heavily influenced by the olfactory system. They focused on high-gamma waves, fast electrical rhythms associated with active neural processing. Slow nasal stimulation increased high-gamma waves in the perirhinal cortex, while fast stimulation decreased them. Higher high-gamma activity correlated with lower anxiety levels.
The scientists traced the pathway of these signals and found that they travel from olfactory sensory neurons in the nose to mitral cells in the olfactory bulb, then to parvalbumin-positive interneurons in the perirhinal cortex, and finally to the basolateral amygdala, a region known for processing fear and anxiety. The researchers noted that the effect was robust, bidirectional (slow input calmed the mice, while fast input increased anxiety), and involved a key relay called long-range projection interneurons in the perirhinal cortex.
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