If you remove most of the salt-craving brain cells, mice no longer seek out salt—even when they’re very low on it.
Scientific Claim
Genetic ablation of approximately 65% of NTSHSD2 neurons in mice abolishes sodium appetite induced by sodium deficiency, demonstrating their necessity for this behavior.
Original Statement
“NTSHSD2 neurons are necessary for sodium appetite... sodium appetite was mostly absent in mice lacking ~65% of their NTSHSD2 neurons.”
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 uses targeted genetic ablation to remove NTSHSD2 neurons and observes a specific, significant loss of sodium appetite, establishing a direct causal necessity within the mouse model.
Evidence from Studies
Supporting (1)
When mice are low on salt, special brain cells called NTSHSD2 neurons turn on and make them want to eat salt—when these cells are disabled, the mice don’t crave salt anymore.