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.

Scientific Claim

NTSHSD2 neurons project monosynaptically to the ventrolateral bed nucleus of the stria terminalis (vlBNST), and optogenetic stimulation of these terminals, but not those in the parabrachial complex, is sufficient to drive sodium appetite in water-restricted mice.

Original Statement

“NTSHSD2 neurons stimulate appetite via projections to the vlBNST, which is also the effector site for ATII-responsive SFO neurons.”

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

Optogenetic stimulation of specific axon terminals with behavioral readouts provides direct causal evidence for the vlBNST as the necessary and sufficient output site for NTSHSD2-driven sodium appetite.

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

Scientists found that certain brain cells sense when the body needs salt and send a direct signal to another brain area that makes mice want to eat salt—this signal works best when a stress hormone is also present.

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

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.

75%

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.

75%

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.

74%

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.

73%

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

71%