Geschatte leestijd: 2 minuten
Many people have a need for salt to give their food just a little more flavor. Researchers have discovered a group of neurons that respond to a lack of salt and have mapped out the process that causes you to crave something salty.
Is the Need for Salt Necessary?
A diet that contains too much salt can lead to high blood pressure and heart disease. Salt is therefore something that we quickly perceive as something bad. However, this once scarce mineral is necessary. It helps regulate fluid balance and plays an important role in regulating blood pressure and cell function throughout the body. When the body loses salt, for example through sweat, hormones are released in response to a salt deficiency. However, it was still unknown how these hormones in the brain cause the behavior to seek salty food.
“Salt Neurons”
Researchers from the Division of Endocrinology, Diabetes and Metabolism at Beth Israel Deaconess Medical Center (BIDMC) have gained more insight into this process. Their findings were published yesterday in Neuron [1]. The team identified a subpopulation of neurons that respond to salt deficiency and mapped out the process in the brain that leads to the subjective need for salt.
An important insight in a world where salt is no longer scarce and many people struggle to limit their salt intake.
We identified a specific circuit in the brain that detects sodium deficiency and drives an appetite specific for sodium to correct the deficiency.In addition, this work establishes that sodium ingestion is tightly regulated by the brain, and dysfunction in these neurons could lead to over- or under consumption of sodium, which could lead to stress on the cardiovascular system over time.
Jon M. Resch, PhD
The team focused on a group of neurons called NTSHSD2, which were discovered ten years earlier by one of the co-authors of the study, Joel Geerlings. In a series of experiments with mice deficient in sodium, the researchers demonstrated that the deficiency in sodium activates these neurons. They also showed that the presence of the hormone aldosterone, which is released in response to a salt deficiency, increases the activity of these neurons.
The researchers also demonstrated that the NTSHSD2 neurons are not the only neurons responsible for the subjective need for salt. In another experiment with mice without salt deficiency, they artificially activated the NTSHSD2. This led to increased salt intake only if signaling of angiotensin II, a hormone also released in response to salt deficiency, occurred simultaneously. Another group of neurons sensitive to angiotensin II should therefore also play a role in the formation of the need for salt. However, these neurons have not yet been identified.
The research shows that only a interplay of the two different groups of neurons that respond to angiotensin II and aldosterone can lead to the immediate need to eat salt. The next step in the research is to determine where angiotensin II in the brain releases its signal.
References
- Jon M. Resch, Henning Fenselau, Joseph C. Madara, Chen Wu, John N. Campbell, Anna Lyubetskaya, Brian A. Dawes, Linus T. Tsai, Monica M. Li, Yoav Livneh, Qingen Ke, Peter M. Kang, Géza Fejes-Tóth, Anikó Náray-Fejes-Tóth, Joel C. Geerling, Bradford B. Lowell. Aldosterone-Sensing Neurons in the NTS Exhibit State-Dependent Pacemaker Activity and Drive Sodium Appetite via Synergy with Angiotensin II Signaling. Neuron, 2017; 96 (1): 190 DOI: 10.1016/j.neuron.2017.09.014
