by New research from a team of scientists in Japan provides insight into how the brain manages the appetite for salt and water. The brain has specific neural circuits that regulate thirst and salt appetite, but the precise mechanisms involved have remained elusive.
Previous studies have shown that the sensation of thirst and salt appetite can be quickly suppressed after ingesting water or salt, even before the substances are absorbed by the digestive system. This suggests the presence of sensing and feedback mechanisms in the digestive organs that modulate thirst and salt appetite in real-time. However, the details of these mechanisms have yet to be fully understood.
To shed light on this topic, the research team focused on the parabrachial nucleus (PBN), which serves as the brain’s relay center for signals related to ingestion from the digestive organs. Using genetically engineered mice, the scientists conducted a series of in vivo experiments. They utilized optogenetic and chemogenetic modifications, as well as in vivo calcium imaging techniques, to visualize and control the activation or inhibition of specific neurons in the lateral PBN (LPBN) using light and chemicals.
During the experiments, the mice were offered water and/or salt water under regular, water-depleted, or salt-depleted conditions. The neural activities and corresponding drinking behaviors were then monitored. Through these experiments, the researchers identified two distinct subpopulations of neurons in the LPBN that responded to water and salt intake. The neuronal population associated with water intake projected from the LPBN to the median preoptic nucleus (MnPO), while the population that responded to salt intake projected to the ventral bed nucleus of the stria terminalis (vBNST).
Notably, when these neuronal populations were artificially activated through optogenetic experiments, the mice drank less water and ingested less salt, even if they had been deprived of water or salt beforehand. Conversely, when the researchers chemically inhibited these neurons, the mice consumed more water and salt than usual. This suggests that these neuronal populations in the LPBN are involved in feedback mechanisms that reduce thirst and salt appetite after water or salt ingestion, helping to prevent excessive intake.
The results of this study, combined with previous neurological research, revealed that the MnPO and vBNST are control centers for thirst and salt appetite. They integrate signals of promotion and suppression from various brain regions, providing a comprehensive understanding of the mechanisms involved.
This research not only contributes valuable insights into the fields of neuroscience and physiology but also has implications for understanding diseases caused by excessive water and salt intake, such as water intoxication, polydipsia, and salt-sensitive hypertension. The lead author of the study, Assistant Professor Takashi Matsuda, explains that unraveling the brain mechanisms controlling water and salt intake behaviors is a significant discovery and paves the way for further research in this area.
Professor Noda, another member of the research team, emphasizes that many neural mechanisms governing fluid homeostasis are still unknown. Further investigation is necessary to understand how the signals for inducing and suppressing water and salt intake, accumulated in the MnPO and vBNST, are integrated and function to control intake behaviors.
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1. Source: Coherent Market Insights, Public sources, Desk research
2. We have leveraged AI tools to mine information and compile it
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