Just turning on the salt-craving brain cells doesn't make mice eat salt fast—unless you also trigger the angiotensin signal, then they immediately start licking salt like crazy.
Scientific Claim
Activation of NTSHSD2 neurons alone does not rapidly induce sodium appetite in mice, but when combined with angiotensin II signaling, it produces rapid and robust sodium consumption, demonstrating a neuronal synergy between aldosterone- and angiotensin-sensitive pathways.
Original Statement
“Remarkably, NTSHSD2 neurons are necessary for sodium appetite, and with concurrent ATII signaling their activity is sufficient to produce rapid consumption.”
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 chemogenetic and pharmacological interventions in mice to demonstrate that NTSHSD2 neuron activation only drives appetite when angiotensin II is present. The causal interaction is directly tested and confirmed.
Evidence from Studies
Supporting (1)
The study found that mice only quickly crave salt when two signals are active at once: one from brain cells that sense aldosterone and another from a hormone called angiotensin II. Neither signal alone makes them eat salt fast — they need both together.