Galvanic vestibular stimulation-induced activation of C1 neurons in medulla oblongata protects against acute lung injury

Autonomic nerves, including the sympathetic and parasympathetic nerves, control the immune system along with their physiological functions. On the peripheral side, the interaction between the splenic sympathetic nerves and immune cells is important for the anti-inflammatory effects. However, the cen...

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Bibliographic Details
Published in:American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2023-02, Vol.324 (2), p.R152-R160
Main Authors: Abe, Chikara, Katayama, Chikako, Ohbayashi, Kento, Horii, Kazuhiro, Ogawa, Bakushi, Fujimoto, Chisato, Iwasaki, Yusaku, Nin, Fumiaki, Morita, Hironobu
Format: Article
Language:English
Subjects:
Acute Lung Injury - prevention & control
Animals
Anti-Inflammatory Agents
Autonomic nervous system
Deletion
Denervation
Electric Stimulation
Hypergravity
Immune system
Inflammation
Injuries
Kidneys
Lungs
Medulla oblongata
Medulla Oblongata - physiology
Mice
Nerves
Neurons
Neurons - physiology
Nitric oxide
Organs
Parasympathetic nervous system
Spleen
Stimulation
Sympathetic nerves
Vestibular system
Vestibule, Labyrinth
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Summary:Autonomic nerves, including the sympathetic and parasympathetic nerves, control the immune system along with their physiological functions. On the peripheral side, the interaction between the splenic sympathetic nerves and immune cells is important for the anti-inflammatory effects. However, the central mechanism underlying these anti-inflammatory effects remains unclear. C1 neurons respond to stressors and subsequently determine the outflow of the autonomic nervous system. We have previously shown that C1 neurons protect against acute kidney injury and found a signaling connection between peripheral vestibular organs and C1 neurons. Thus, we hypothesized that hypergravity load or galvanic vestibular stimulation (GVS) might protect against acute lung injury. We showed that C1 neurons are histologically and functionally activated by stimulating the peripheral vestibular organs. Protection against acute lung injury that was induced by a 2 G load disappeared due to vestibular lesions or the deletion of C1 neurons. This GVS-induced protective effect was also eliminated by the deletion of the C1 neurons. Furthermore, GVS increased splenic sympathetic nerve activity in conscious mice, and splenic sympathetic denervation abolished the GVS-induced protection against acute lung injury. Therefore, the activated pathway between C1 neurons and splenic sympathetic nerves is indispensable for GVS-induced protection against acute lung injury.
ISSN:0363-6119
1522-1490
DOI:10.1152/ajpregu.00131.2022