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Stony Brook University Researchers Uncover Neural Mechanisms Behind Taste Sensitivity
Researchers at Stony Brook University have identified a neural mechanism that influences sweet taste preference. Their study, published in Current Biology, demonstrates how neurosteroids—chemical signals involved in mood regulation and stress—can reduce sensitivity and preference for sweet tastes when elevated in the gustatory cortex, the brain region responsible for taste perception.
The Link Between Brain Activity and Taste Preference
According to senior author Dr. Arianna Maffei, a professor in the Department of Neurobiology and Behavior, studies suggest that food preferences influence eating habits, and reduced taste sensitivity is often linked to overconsumption, potentially leading to obesity. However, understanding how brain activity contributes to variations in taste preference has remained challenging due to technological limitations in measuring brain changes at a high resolution in humans.
To overcome this challenge, the researchers turned to laboratory mice, whose biology of taste closely resembles that of humans. This approach allowed them to monitor brain activity while measuring taste preferences in a controlled environment.
Investigating the Role of Neurosteroids
The research team focused on allopregnanolone, a neurosteroid known to be elevated in individuals affected by obesity. This neurosteroid modulates brain activity by increasing tonic inhibitory circuits via a specific type of GABA receptor.
Their findings revealed that these GABA receptors are present in both excitatory and inhibitory neurons within the gustatory cortex. To explore their function, the scientists infused allopregnanolone directly into the gustatory cortex of mice, leading to a noticeable reduction in sweet taste sensitivity and preference.
Further, they employed genetic tools to remove neurosteroid-sensitive GABA receptors from the gustatory cortex. This genetic manipulation eliminated the mice’s preference for sweet taste over water. The effect was even more pronounced when receptors were selectively removed from inhibitory neurons—these mice were virtually unable to distinguish sugared water from plain water.
Implications and Future Research
These findings confirm that a specific type of GABA receptor is a target for neurosteroid activity and plays a crucial role in fine-tuning sweet taste sensitivity. Dr. Maffei emphasizes that their research illustrates the intricate ways in which the mammalian brain contributes to the taste experience and highlights a key neural signal essential for sweetness perception.
Ongoing research aims to determine whether neurosteroids regulate sensitivity to other tastes beyond sweetness and how changes in taste sensitivity might impact eating behaviors. These insights could have important implications for understanding and addressing eating disorders and obesity-related conditions.
For further details, refer to the full study: Priscilla E. Yevoo et al, “Modulation of sweet preference by neurosteroid-sensitive, δ-GABAA receptors in adult mouse gustatory insular cortex,” Current Biology (2025). DOI: 10.1016/j.cub.2025.01.035
Disclaimer: This article is based on scientific research and is intended for informational purposes only. Further studies are required to confirm these findings in humans, and medical professionals should be consulted before making any dietary or health-related decisions based on this research.
