Food consumption can be turned off in mice by silencing neurons in a particular brain area. Credit: Ricardo Ribas/SOPA Images/LightRocket/Getty
Scientists have identified a ‘brain dial’ that can turn food consumption on or off, at least in mice. The effect of this brain region is so powerful that when scientists manipulated it, mice that were already full kept eating — and even gobbled inedible plastic pellets.
The region receives and coordinates multiple streams of information, such as hunger levels, nutritional deficits and whether a food is pleasurable to eat. It is a “key hub” linking the sensory traits of food to weight control — a finding with implications for human health, according to a paper published on 10 September in Cell1.
“I am deeply impressed by this study,” says Matthew Carter, a neuroscientist at Williams College in Williamstown, Massachusetts, who was not involved in the research. The work is unusual in separating out how hunger and a food’s sensory qualities affect food consumption, he says, and demonstrates that a single brain region integrates a range of signals to drive consumption.
The bitter with the sweet
Food intake is influenced by roughly a dozen brain regions. These areas gather information on various factors that together drive our appetite for something and how likely we are to consume it. A person low on salt might crave a salty snack, for example, but decline something bitter. In 2019, researchers suggested that all of these stimuli might be funnelled into a brain region called the bed nucleus of the stria terminalis (BNST)2, but it remained unclear what exactly was happening inside.
Charles Zuker, a neuroscientist at Columbia University in New York City, and his team wanted to trace the brain circuits involved in an animal’s response to tastes. The researchers began by characterizing neurons that become active when a mouse tastes something sweet. In the central amygdala and hypothalamus, they found sweet-detection neurons with branches that link to neurons in the BNST.
How we taste sweetness: long-sought structure of human receptor mapped at last
When the scientists silenced those BNST neurons, the animals lost their interest in sugar even when hungry, and largely ceased to eat. The researchers also activated those BNST neurons in mice that had recently been fed and so shouldn’t seek out food. Nevertheless, the activation prompted the mice to ingest all kinds of things: water (a neutral substance they would typically ignore unless thirsty), salt, fat, bitter substances and even plastic pellets.
Collectively, these and other results “tell us that the BNST is functioning as something of a master ‘dial’ with bidirectional control”, Zuker says. “If we can figure out how to turn that dial, it would give us some influence over things like body weight.”