The study, published in Cell, identifies neurons in the central amygdala connected to the BNST that influence feeding by either amplifying or suppressing the desire to eat, with activation of BNST neurons increasing food consumption.

Particularly, taste signals like sweet tastes activate neurons in the amygdala that then stimulate BNST neurons, further promoting eating.

The research demonstrates that stimulating BNST neurons causes mice to eat even when full and to consume inedible objects, providing insight into how this brain region controls feeding.

These findings suggest that targeting the BNST could have therapeutic potential for conditions like cachexia in chemotherapy patients, who suffer from severe appetite loss and weight decline.

The study also uncovered anatomical connections between the BNST and other brain circuits that monitor internal states like hunger and salt deficiency, highlighting how the brain integrates internal needs with sensory signals to regulate consumption.

Additionally, the research indicates that the weight-loss drug semaglutide targets neurons in the BNST, offering insights into its mechanism and potential for developing appetite-suppressing therapies with fewer side effects.

Scientists at Columbia University's Zuckerman Institute have identified a previously unknown brain region in mice called the bed nucleus of the stria terminalis (BNST), which acts as a master regulator of feeding behavior, influencing the consumption of sugars, fats, salts, and other dietary components.

Further research has revealed that the BNST functions as a 'brain dial' that can switch food consumption on or off, effectively controlling the urge to eat various foods.

This discovery was made possible through advanced techniques like optogenetics and anatomical tracing, mapping the BNST's role and connectivity within the brain.

The findings demonstrate that activating BNST neurons causes mice to eat even when full and to consume inedible objects like plastic pellets, highlighting its powerful influence over feeding behavior.

The research also shows that the BNST integrates multiple signals related to hunger, nutritional deficits, and food pleasure, serving as a key hub linking sensory food traits to weight control.

In experiments, more BNST neurons respond to sweet and salty tastes in hungry or salt-depleted mice compared to satiated ones, indicating the BNST's role in integrating hunger and nutrient signals to regulate eating behavior.