Suffolk Reporter

Researchers at Stony Brook University have discovered a specific signal in the brain that may influence the preference for sweet foods. The study, published in Current Biology, used genetic manipulation in laboratory models to explore how neurosteroids affect taste sensitivity and preference.

Senior author Arianna Maffei, PhD, a professor in the Department of Neurobiology and Behavior, noted that human studies suggest food preferences impact consumption levels, which can lead to obesity when taste sensitivity decreases. However, identifying biological mechanisms in humans is challenging due to technological limitations.

The research team studied neural circuits related to sweet taste preference using mice models. They focused on allopregnanolone, a neurosteroid linked to obesity. This substance affects brain activity by modulating inhibitory circuits through GABA receptors present in neurons within the gustatory cortex.

By infusing allopregnanolone into the mice's gustatory cortex, researchers activated these GABA receptors, reducing sensitivity and preference for sweet tastes. Genetic tools were then used to remove these receptors locally, further diminishing the mice's ability to prefer sweet over water.

“This reduced sensitivity and preference for sweet taste was even more prominent if the receptors were selectively removed only from inhibitory gustatory cortex neurons. Indeed, in this case mice were practically unable to distinguish sugared water from water,” explains Maffei.

The study confirmed that specific GABA receptors are crucial for adjusting sweet taste sensitivity and preference. Maffei highlighted that their findings reveal significant insights into how the mammalian brain influences taste experiences.

Further research is underway to determine whether neurosteroids regulate other taste sensations or how changes in taste sensitivity affect eating habits.

This research received support from various grants provided by the National Institute for Deafness and Communication Disorder (NIDCD) branch of the National Institutes of Health (NIH), including grants R01DC019827, R01DC013770, R01DC015234, F31 DC019518 and UF1NS115779. The authors are affiliated with Stony Brook University's College of Arts and Science and Renaissance School of Medicine.