By activating a neuron in the prefrontal cortex of a mouse's brain, scientists are able to make the mouse eat more. But what could this mean for humans?
The influence that different areas of the brain may have over eating behaviors is a contentious debate in neurobiology.
"Researchers tend to be either in a camp that believes the control of eating is all regulated from the top down, or from the bottom up," says Ralph DiLeone, senior author of the paper, referring to whether it is "higher" decision-making areas of the brain or more "primitive" brain functions that regulate eating behaviors.
"Both are important and this paper brings a little more neurobiological clarity to the question," DiLeone claims.
In 2012, Medical News Today reported on a study suggesting that fructose increases activity in the hypothalamus, insula and striatum - areas of the brain responsible for processing motivation and reward. Fructose prevented certain brain cells that instruct us to eat from telling us we are full, and so seemed to increase "food-seeking behavior."
Another 2012 study suggested that a brain receptor called Gpr17 has a role in controlling appetite, and that this could form the basis of potential new anti-obesity medications.
The new study, published in the journal Nature Neuroscience, focuses on the prefrontal cortex - a decision-making area of the brain, which some scientists had suspected may play a role in the eating behaviors of mammals.
Scientists have so far been unable to account for how this relationship between the prefrontal cortex and appetite regulation might work, though.
Switching off neurons prompted mice to eat less
Dopamine, the neurotransmitter that controls the reward and pleasure centers of the brain, is also known to have an important function in food intake.
Activating the D1 dopamine-receptor neurons caused the mice to eat more.
Dopamine allows our brain to perceive rewards and to take steps to move toward them. When animals have low levels of dopamine in their brain, they stop eating and eventually die from starvation.
The researchers activated the D1 dopamine-receptor neurons in the prefrontal cortex of mice. They found that this caused the mice to eat more, while inhibiting - or "switching off" - the same neurons caused the mice to eat less.
The dopamine pathway toggled on and off by the scientists in this study also intersects with areas of the brain, such as the amygdala, which process emotional responses.
The researchers think that this could mean eating behavior is regulated at the junction between the decision-making and more primitive emotion centers of the brain.
The authors think that this region of brain circuitry could provide the key to new medication for regulating eating behavior:
"This circuit presents new therapeutic opportunities, as future interventions for obesity or eating disorders may consider this prefrontal circuit for pharmacotherapy."