The human brain regulates water and salt appetite to maintain proper hydration. A new study published in Cell Reports reveals how the brain’s centre for digestive signals has two distinct neuronal populations that regulate either salt or water intake.
Previous studies suggested that water or salt ingestion quickly suppresses thirst and salt appetite before the digestive system absorbs the ingested substances, indicating the presence of sensing and feedback mechanisms in digestive organs that help real-time thirst and salt appetite modulation in response to drinking and feeding. Unfortunately, despite extensive research on this subject, the details of these underlying mechanisms remained elusive.
To shed light on this matter, a research team from Japan has recently conducted an in-depth study on the parabrachial nucleus (PBN), the brain’s relay centre for ingestion signals coming from digestive organs.
The researchers conducted a series of in vivo experiments using genetically engineered mice.
They introduced optogenetic (and chemogenetic) modifications and in vivo calcium imaging techniques into these mice, enabling them to visualise and control the activation or inhibition of specific neurons in the lateral PBN (LPBN) using light (and chemicals). During the experiments, the researchers offered the mice, either in regular or water- or salt-depleted conditions, water and/or salt water, and monitored neural activities along with the corresponding drinking behaviours.
In this way, the team identified two distinct subpopulations of cholecystokinin mRNA-positive neurons in the LPBN, which underwent activation during water and salt intake.
The neuronal population that responds to water intake projects from the LPBN to the median preoptic nucleus (MnPO), whereas the one that responds to salt intake projects to the ventral bed nucleus of the stria terminalis (vBNST). Interestingly, if the researchers artificially activated these neuronal populations through optogenetic (genetic control using light) experiments, the mice drank substantially less water and ingested less salt, even if they were previously water- or salt-deprived.
Similarly, when the researchers chemically inhibited these neurons, the mice consumed more water and salt than usual.
Therefore, these neuronal populations in the LPBN are involved in feedback mechanisms that reduce thirst and salt appetite upon water or salt ingestion, possibly helping prevent excessive water or salt intake.
These results, alongside their previous neurological studies, also reveal that MnPO and vBNST are the control centres for thirst and salt appetite, integrating promotion and suppression signals from several other brain regions.
“Understanding brain mechanisms controlling water and salt intake behaviours is not only a significant discovery in the fields of neuroscience and physiology, but also contributes valuable insights to understand the mechanisms underlying diseases induced by excessive water and salt intake, such as water intoxication, polydipsia, and salt-sensitive hypertension,” remarks first author, Assistant Professor Takashi Matsuda from Tokyo Institute of Technology.
Source: Tokyo Institute of Technology
