When the body is low on salt, special cells in the brainstem that detect this imbalance send a 'go' signal to the salt-craving neurons, turning them on.
Scientific Claim
In sodium-depleted mice, excitatory inputs from HSD2-expressing neurons in the nucleus of the solitary tract are necessary and sufficient to activate pre-locus coeruleus prodynorphin neurons and drive sodium appetite.
Original Statement
“A majority of recorded pre-LCPDYN neurons received monosynaptic excitatory inputs from NTSHSD2 neurons... optogenetic stimulation of NTSHSD2 neurons activated pre-LCPDYN neurons in sated animals... ablation of NTSHSD2 neurons greatly attenuated c-Fos expression in pre-LCPDYN neurons after sodium-depletion.”
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 circuit mapping, optogenetic activation, and targeted ablation to demonstrate that NTSHSD2 inputs are both necessary and sufficient to drive pre-LC PDYN activity in mice, supporting definitive causal claims within the model.
Evidence from Studies
Supporting (0)
Contradicting (1)
Chemosensory modulation of neural circuits for sodium appetite
The study found a brain circuit that makes mice crave salt, but it didn’t look at the specific brain cells the claim says start the craving, so we can’t say if the claim is right or wrong.