Study links brain signals with sweet food attraction


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

Arianna Maffei, PhD, Professor in the Department of Neurobiology and Behavior, explained that human studies suggest food preferences impact consumption levels and decreased taste sensitivity is linked to overconsumption, potentially leading to obesity. However, understanding brain activity's role in taste preference differences remains challenging due to technological limitations.

In their research using mice, the team focused on neural circuits related to sweet taste preference. They examined the neurosteroid allopregnanolone, known for its elevated presence in individuals with obesity. This neurosteroid influences brain activity by increasing tonic inhibitory circuits through a specific type of GABA receptor found in neurons within the gustatory cortex.

The researchers infused allopregnanolone into the mice's gustatory cortex to activate these receptors, reducing their sensitivity and preference for sweet tastes. By removing neurosteroid-sensitive GABA receptors from this region using genetic tools, they eliminated the mice's preference for sweet taste 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.

Their findings confirm that a specific type of GABA receptor is crucial for modulating sensitivity and preference for sweet tastes. The ongoing research aims to determine whether neurosteroids also regulate other taste sensations or influence eating habits through changes in taste sensitivity.

The study received support from several 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.

Authors involved are affiliated with Stony Brook University's College of Arts and Science (Yevoo and Maffei) as well as the Renaissance School of Medicine (Fontanini).

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