When mice are low on salt, certain brain cells in the back of the brain start firing on their own like a heartbeat, thanks to special sodium channels, and this makes them crave salt.

Scientific Claim

In sodium-deficient mice, NTSHSD2 neurons in the nucleus of the solitary tract exhibit spontaneous pacemaker-like firing at approximately 2–3 Hz, driven by the synergistic interaction of HCN channels and the TTX-resistant Nav1.5 sodium channel, which are upregulated during sodium deficiency and are necessary for sodium appetite.

Original Statement

“NTSHSD2 neurons respond to sodium deficiency with spontaneous pacemaker-like activity—the consequence of 'cardiac' HCN and Nav1.5 channels.”

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

Evidence Quality Assessment

Claim Status

appropriately stated

Study Design Support

Design supports claim

Appropriate Language Strength

definitive

Can make definitive causal claims

Assessment Explanation

The study directly measures neuronal firing and channel activity in mice using controlled electrophysiology and genetic tools. The causal link between channel activity and firing is demonstrated through pharmacological blockade and ablation, justifying definitive language within the mouse model.

Evidence from Studies

Supporting (1)

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

When mice are low on salt, certain brain cells start firing on their own like a heartbeat, thanks to two special channels that become more active — and this tells the mice to go find and eat salt.

Contradicting (0)

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

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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The brain uses two different signals to control salt craving: one slow signal that says 'we need salt' and one fast signal that says 'you tasted salt, stop now'—and they work together to make the mouse eat just enough.

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Only the salt-sensing brain cells get more active when salt is low—not other nearby cells—and they don’t get the signal from nerves in the gut, meaning they respond directly to hormones in the blood.

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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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