By GREGORY ZELLER //
Cookie craving? Hankering for a Hershey’s bar? Screaming for ice cream? It’s all in your mind.
That’s a literal truth, according to Stony Brook University researchers who genetically manipulated a laboratory brain model to demonstrate how mental signals regulating mood and stress affect our sensitivity to (and desire for) sweet treats – a significant advance on the road to understanding, and ultimately defeating, obesity.
Welcome to the gustatory complex, a multimodal brain region heavily involved with taste and, according to modern science, one of the least understood of the human animal’s primary sensory cortices.
It’s also ground zero for our attraction to certain foods, notes SBU Department of Neurobiology and Behavior Professor Arianna Maffei, especially those sweet tastes we all occasionally crave.
Alfredo Fontanini: Sweet dreams.
In “Modulation of Sweet Preference by Neurosteroid-Sensitive δ-GABAA Receptors in Adult Mouse Gustatory Insular Cortex,” a mouthful of a study published this week in the open-access scientific journal Current Biology, Maffei and her research team discuss their genetic-manipulation discoveries – primarily, that decreased sensitivity to taste is directly related to overconsumption, which routinely leads to obesity.
Determining the relationship between brain activity, taste preferences and eating habits in humans has been historically difficult – contemporary technologies for measuring brain activity lack sufficient resolution for identifying specific biological mechanisms.
But scientists can accurately monitor brain activity in lab mice, while also measuring their taste preferences.
And as the biology of taste is similar in all mammals, Maffei and her team – including fellow Neurobiology and Behavior Professor Alfredo Fontanini, visiting from Italy’s Universita’ degli Studi di Brescia, and graduate research assistant Priscilla Yevoo – were able to shed new light on the human brain’s role in taste preferences and eating habits.
In short: The new study is a virtual smorgasbord of useful information about what’s really going on in the gustatory complex.
The team focused on the effects of allopregnanolone, a neurosteroid spun out of the mammalian sex hormone progesterone. Allopregnanolone, which is known to be elevated in obese persons, modulates brain activity “circuits” controlled by a specific type of acid receptor found in gustatory complex neurons – specifically, neurons that either excite or inhibit the complex.
Let them eat cake: Turns out mice crave sweets pretty much the same way you do.
By tinkering with allopregnanolone levels, the researchers were able to first reduce the mouse model’s sensitivity to (and preference for) sweet tastes – and then eliminate the rodent’s preference for sweet taste altogether.
“This reduced sensitivity and preference for sweet taste was even more prominent if the receptors were selectively removed only from inhibitory gustatory cortex neurons,” Maffei noted. “In this case, mice were practically unable to distinguish sugared water from water.”
This confirmed that the acid receptor modulating those circuits in gustatory complex neurons is a focal point for neurosteroid activity – and essential for fine-tuning a mammal’s preference for sweet tastes.
The study – supported by several grants from the National Institutes of Health’s National Institute for Deafness and Communication Disorder – confirms something only hypothesized before now: A specific signal in a specific brain region is essential to mammalian sensitivity to sweetness.
And it’s only a first step, according to Maffei: Ongoing research models will explore whether neurosteroids regulate only sweet-taste sensation or contribute to the perception of other tastes as well – and, ultimately, how changes in taste sensitivity influence human eating patterns.
