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Finally some answers about where your salt cravings come from

A diet high in salt may be most commonly associated with high blood pressure and cardiovascular disease, but the reality is that the body needs salt to balance its water content, control blood pressure, and regulate cellular function. As the body loses salt, hormones are released in response to sodium deficiency. New research is unraveling the mystery of how these hormones influence the brain, causing increased salt cravings and consumption.

A team of scientists at the Beth Israel Deaconess Medical Center (BIDMC) have  identified neurons that respond to the body’s sodium deficiency. As a result, they managed to map the brain circuitry that drives salt-seeking behavior.

“We identified a specific circuit in the brain that detects sodium deficiency and drives an appetite specific for sodium to correct the deficiency,” said co-author Jon M. Resch. “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.”

The team focused on a subset of neurons known as NTSHSD2. Through a series of experiments on sodium-deficient mice, the researchers managed to show that sodium deficiency activates these neurons. They also found that the presence of aldosterone, the hormone which is released during sodium deficiency, increases the response of these neurons.

“These neurons appear to be highly influenced by these hormones and less so by inputs from other neurons – though further study is warranted,” said Resch. “This is a unique and very unexpected feature of these NTSHSD2 neurons.”

Further evaluation of mice that were not deficient in sodium showed that the activation of NTSHSD2 neurons only triggered sodium consumption when there was a simultaneous signaling by another hormone released during sodium deficiency, angiotensin II. Because of this, the team established that NTSHSD2 neurons are not solely responsible for driving the sodium appetite. This second set of neurons, which have not yet been identified, most likely play a role in the drive for salt consumption as well.

“Several questions remain with regard to how sodium appetite works, but a major one is where ATII is acting in the brain and how the signal works in concert with NTSHSD2 neurons that respond to aldosterone,” said Resch. “We have already begun work to help us close these gaps in our knowledge.”

The research is published today in the journal Neuron.

By Chrissy Sexton, Staff Writer

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