When mice taste salt, a different group of brain cells that use a calming chemical (GABA) gets turned on and sends a 'stop' signal to the salt-craving cells, making them quiet down.
Scientific Claim
In sodium-depleted mice, GABAergic neurons in the dorsal bed nucleus of the stria terminalis that express prodynorphin are activated by sodium taste and send direct inhibitory projections to pre-locus coeruleus prodynorphin neurons to mediate rapid satiety.
Original Statement
“Retrograde-virus tracing showed that sensory modulation is in part mediated by specific GABA-producing neurons in the bed nucleus of the stria terminalis... dBNSTPDYN neurons send monosynaptic inhibitory inputs to pre-LCPDYN neurons... dBNST→ pre-LC neurons responded upon NaCl intake... strongly inhibited by amiloride.”
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 monosynaptic rabies tracing, optogenetic validation, and in vivo calcium imaging to establish a direct, functional inhibitory connection between dBNST and pre-LC neurons in mice, justifying definitive language.
Evidence from Studies
Supporting (1)
Chemosensory modulation of neural circuits for sodium appetite
When mice are low on salt, tasting salt turns off brain cells that make them crave more salt, and this happens because a specific group of brain cells that use GABA sends a 'stop' signal to the craving cells.