It’s not just being thirsty that makes mice eat salt—only when the angiotensin signal is present does turning on salt-craving cells make them lick salt, not when they’re just dehydrated.

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Evidence from Studies

Supporting (1)

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Aldosterone-Sensing Neurons in the NTS Exhibit State-Dependent Pacemaker Activity and Drive Sodium Appetite via Synergy with Angiotensin II Signaling.

Cohort Study

Animal

2017 Sep 27

The study shows that your brain needs two signals together—angiotensin II and active NTSHSD2 neurons—to make you crave salt. Just making you thirsty with salty water doesn’t trigger salt cravings, even if those brain cells are active, which means it’s not about thirst—it’s a special salt-craving system.

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No contradicting evidence found

Source Study

Aldosterone-Sensing Neurons in the NTS Exhibit State-Dependent Pacemaker Activity and Drive Sodium Appetite via Synergy with Angiotensin II Signaling.

Score: 11

DOI: 10.1016/j.neuron.2017.09.014

Similar Assertions

Just turning on the salt-craving brain cells doesn't make mice eat salt fast—unless you also trigger the angiotensin signal, then they immediately start licking salt like crazy.

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The same brain cells that sense low salt also have a built-in alarm for angiotensin, a hormone that signals low blood volume—so they respond to both signals together.

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The salt-craving brain cells connect directly to a specific spot in the brain called the vlBNST—turning on just that connection makes mice drink salt water, even without other triggers.

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If you remove most of the salt-craving brain cells, mice no longer seek out salt—even when they’re very low on it.

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