Overview

• Activating BNST neurons drove even sated mice to keep consuming—including bitter solutions and plastic pellets—while silencing the circuit sharply reduced intake.
• Sweet-selective neurons in the central amygdala project to and activate the BNST, establishing a defined pathway by which taste information reaches this hub.
• More BNST cells responded to sweet or salty cues when mice were hungry or salt-depleted, indicating integration of internal physiological needs with sensory inputs.
• Stimulating the BNST protected mice from chemotherapy-associated weight loss in a cachexia-like model, pointing to potential ways to support appetite during treatment.
• The GLP-1 drug semaglutide targets BNST neurons, offering clues to how current weight-loss medicines suppress consumption, though relevance to humans remains to be validated.