If you block the salt taste receptors in a mouse’s mouth, it can’t tell it’s tasted salt—so its brain doesn’t stop craving salt, even if it’s had enough.

Scientific Claim

In sodium-depleted mice, the suppression of pre-locus coeruleus prodynorphin neurons by oral sodium is dependent on the epithelial sodium channel (ENaC), as pharmacological blockade with amiloride abolishes both neuronal inhibition and satiety.

Original Statement

“Blocking the sodium taste receptor by amiloride fully abolished NaCl-induced suppression of pre-LCPDYN neurons... dBNST→ pre-LC neurons responded upon NaCl intake... strongly inhibited by amiloride.”

From study:Chemosensory modulation of neural circuits for sodium appetite

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 pharmacological blockade (amiloride) to demonstrate a direct, necessary role for ENaC in both neuronal suppression and behavioral satiety, supporting definitive causal claims within the mouse model.

Evidence from Studies

Supporting (0)

No supporting evidence found

Contradicting (1)

Chemosensory modulation of neural circuits for sodium appetite

Cohort Study

Animal

2019 Apr

The study shows that tasting salt turns off brain cells that make mice crave salt, but it doesn’t say whether a specific salt-sensing molecule (ENaC) is responsible — so we can’t confirm the claim about amiloride blocking it.

Source Study

Chemosensory modulation of neural circuits for sodium appetite

Score: 12

DOI: 10.1038/s41586-019-1053-2

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