A research group led by Takashi Matsuda, a specially appointed assistant professor, and Masaharu Noda, a specially appointed professor of the Institute of Bioconstancy Research, Institute of Science and Technology, Tokyo Institute of Technology, identified nerve cells that suppress water intake in the brain and regulated thirst. For the first time, we have clarified the mechanism of new brain function.
In vertebrates, including humans, the sodium ion concentration in body fluids remains constant.This is called fluid homeostasis and is essential for life support, and proper control of drinking behavior is very important for this.Excessive suppression or excessive fluid intake resulting from abnormal mouth thirst causes some pathology and causes fatal damage to many organs including the brain.However, there were many unclear points about the mechanism of suppressing drinking behavior.
Using mice, the research group identified nerve cells (CCK-operated neurons) that secrete cholecystokinin, a neurotransmitter, in the subfornical organs (organs involved in water / salt intake and blood pressure control) in the brain.It was clarified that the activation of these CCK neurons suppresses drinking behavior.We also found that there are two types of CCK neurons: a population that is continuously activated in response to a decrease in sodium ion concentration in body fluids, and a population that is transiently activated in response to drinking behavior.Furthermore, using optogenetics, we controlled the artificial activity of each CCK neuron and succeeded in controlling the drinking behavior of mice.
So far, the research group has clarified the nerve cells (water neurons) that control the induction of drinking behavior in the subfornical organ and their neural circuits.This time, we elucidated the mechanism of activity regulation of water neurons for the first time.It is expected to contribute to the establishment of treatment and prevention methods for diseases induced by excessive fluid intake, such as water intoxication and polydipsia caused by abnormal mouth thirst.
Paper information:[Nature Communications] Distinct CCK-positive SFO neurons are involved in persistent or transient suppression of water intake