MOLECULAR AND NEURAL MECHANISMS OF THE DIVING RESPONSE

The diving response (DR) is a coordinated autonomic reflex that allows mammals to survive in extreme environments such as under water by decreasing heart rate, stopping respiration, and constricting blood vessels when oxygen is not available. It is known that the physiological mechanism of DR involves the trigeminal nerve and the medulla, but the molecular and neural mechanisms underlying the reflex remain unclear. Sensory receptors found on the trigeminal nerve are of particular interest, such as the cold-sensing receptor, transient receptor potential melastatin (TRPM8). Our research aims to understand the role of sensory receptors and the brain circuits involved in DR in mice. First, we stimulated the nose of wild-type (C57BL/6) mice with water-soaked cotton and recorded their heart rate with an electrocardiogram (ECG). We found that they exhibited a decreased heart rate with this stimulus. Next, we tested the same stimulus to TRPM8 heterozygous and homozygous knockout mice and found that they showed changes in heart rate similarly to wild-type mice, suggesting that TRPM8 alone may not be essential for the initiation of DR. Then, we conducted c-Fos labeling on wild-type mice and found activation of the piriform cortex, pontine nucleus, nucleus of the solitary tract (NTS), and rostral ventrolateral medulla (RVLM) following DR stimuli. Future experiments will focus on other sensory receptors to determine its involvement in the DR. The findings will contribute to understanding how mammals maintain their homeostasis via autonomic nervous system in extreme environments.