It’s not just being thirsty that makes mice eat salt—only when the angiotensin signal is present does turning on salt-craving cells make them lick salt, not when they’re just dehydrated.
Scientific Claim
The synergy between angiotensin II and NTSHSD2 neuron activation to drive sodium appetite is specific to angiotensin signaling and not due to thirst, as hyperosmotic thirst-inducing stimuli fail to enable salt appetite even when NTSHSD2 neurons are activated.
Original Statement
“To confirm the role of ATII signaling... neither NaCl nor sucrose, unlike H2O restriction, enabled increased consumption of 3% NaCl in response to NTSHSD2 neuron 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 directly compares two types of thirst (angiotensin-mediated vs. osmotic) and shows only the former enables salt appetite with NTSHSD2 activation, providing strong evidence for specificity.
Evidence from Studies
Supporting (1)
The study shows that your brain needs two signals together—angiotensin II and active NTSHSD2 neurons—to make you crave salt. Just making you thirsty with salty water doesn’t trigger salt cravings, even if those brain cells are active, which means it’s not about thirst—it’s a special salt-craving system.