When mice are low on salt, a specific group of brain cells makes them desperately want to eat salt—even if it tastes bad—and these cells also make the mice feel bad, so they do things to stop the feeling.
Scientific Claim
In sodium-depleted mice, activation of prodynorphin-expressing excitatory neurons in the pre-locus coeruleus drives robust ingestion of sodium, even from aversive sources like rock salt, and these neurons encode an aversive motivational state that animals work to terminate.
Original Statement
“Acute stimulation of this population triggered robust sodium ingestion even from rock salt... photostimulation of pre-LCPDYN neurons significantly reduced occupancy time in the compartment paired with light... animals exhibited robust lever-press behavior to stop stimulation.”
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 precise genetic targeting, optogenetic activation/inhibition, and behavioral assays in mice to establish a direct, causal-like role for these neurons in sodium intake and aversion within the experimental model. Definitive language is appropriate for describing neural circuit function in this controlled animal model.
Evidence from Studies
Supporting (1)
Chemosensory modulation of neural circuits for sodium appetite
When mice are low on salt, special brain cells make them really want to eat salt—even if it tastes bad—because those cells feel unpleasant. Eating salt, even just tasting it, turns off those cells and makes them feel better.