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Summary: Researchers identified a brain circuit in mice that drives them to search for food even when they are not hungry, focusing on a specific group of cells in the periaqueductal gray (PAG) area of the brain stem. This discovery highlights how stimulation of these cells causes mice to prefer high-calorie foods and engage in food-seeking behaviors, regardless of hunger.
The study suggests that humans possess similar cells, offering potential new insights into eating disorders. By manipulating the activity of these cells, the researchers demonstrated the ability to increase or decrease foraging behavior in mice, pointing to possible future treatments for binge eating and anorexia in humans.
Key facts:
- Specific brain cells drive the search for food: The researchers found that stimulation of vgat PAG cells in mice leads to food-seeking behavior, even in the absence of hunger, highlighting a distinction between craving high-calorie foods and actual hunger.
- Implications for eating disorders: The presence of similar cells in humans suggests that hyperactivity or hypoactivity in this brain circuit could contribute to disorders such as binge eating and anorexia, making it a potential target for treatment.
- Compulsive consumption of high-calorie foods: Mice activated by these cells demonstrated a preference for fatty and sugary foods over healthier options, indicating the circuit’s role in the desire for highly rewarding foods.
Fountain: UCLA
People who find themselves rummaging through the refrigerator for a snack soon after eating a large meal may have overactive food-seeking neurons, not an overactive appetite.
UCLA psychologists have discovered a circuit in the brains of mice that makes them crave and seek food, even when they are not hungry. When stimulated, this group of cells drives mice to forage vigorously and to prefer fatty, indulgent foods like chocolate over healthier foods like carrots.
People have the same cell types and, if confirmed in humans, the finding could offer new ways to understand eating disorders.
The report, published in the magazine Nature Communicationsis the first to find cells dedicated to foraging in a part of the mouse brainstem usually associated with panic, but not feeding.
“This region we are studying is called periaqueductal gray (PAG) and it is in the brainstem, which is very old in evolutionary history and so is functionally similar between humans and mice,” said corresponding author Avishek Adhikari. , associate professor of psychology at UCLA.
“Although our findings were a surprise, it makes sense that foraging has its roots in such an ancient part of the brain, since foraging is something all animals must do.”
Adhikari studies how fear and anxiety help animals evaluate risks and minimize exposure to threats, and his group made the discovery while trying to learn how this particular location was involved in fear.
“Activation of the entire PAG region causes a dramatic panic response in both mice and humans. But when we selectively stimulated only this specific group of PAG neurons called vgat PAG cells, they did not alter fear and instead caused foraging and feeding,” Adhikari said.
The researchers injected mouse brains with a genetically modified virus to cause brain cells to produce a light-sensitive protein. When a laser shines on cells through a fiber optic implant, the new protein translates that light into electrical neuronal activity in the cells. A miniature microscope, developed at UCLA and attached to the mouse’s head, recorded the cells’ neuronal activity.
When stimulated with laser light, vgat PAG cells fired, sending the mouse chasing live crickets and food other than its prey, even if it had just eaten a large meal. The stimulation also prompted the mouse to follow moving objects that were not food (such as ping pong balls, although it did not try to eat them) and also prompted the mouse to confidently explore everything in its enclosure.
“The results suggest that the following behavior is more related to desire than hunger,” Adhikari said.
“Hunger is aversive, meaning that mice typically avoid feeling hungry if they can. But they look for activation of these cells, which suggests that the circuit is not causing hunger. Instead, we believe this circuit triggers cravings for highly satisfying, high-calorie foods. “These cells can make the mouse eat more high-calorie foods even in the absence of hunger.”
Sated mice with activated vgat PAG cells craved fatty foods so much that they were willing to endure foot-tapping to get them, something sated mice normally wouldn’t do. In contrast, when the researchers injected a virus designed to produce a protein that dampens cell activity under light exposure, the mice searched for food less, even if they were very hungry.
“Mice show binge eating in the presence of direct aversive consequences when this circuit is active, and do not seek food even if they are hungry when it is not active. “This circuit can bypass normal hunger pressures on how, what and when to eat,” said Fernando Reis, a UCLA postdoctoral researcher who performed most of the experiments in the paper and came up with the idea of studying binge eating.
“We are conducting new experiments based on these findings and learning that these cells induce the consumption of fatty and sugary foods, but not vegetables in mice, suggesting that this circuit may increase consumption of junk food.”
Like mice, humans also possess vgat PAG cells in the brainstem. It could be that if this circuit is overactive in a person, they feel more rewarded when eating or crave food when they are not hungry. Conversely, if this circuit is not active enough, they may feel less pleasure associated with food, which could contribute to anorexia. If found in humans, the food-seeking circuit could become a treatment target for some types of eating disorders.
Money: The research was supported by the National Institute of Mental Health, the Brain & Behavior Research Foundation, and the National Science Foundation.
About this research news on hunger and neuroscience
Author: Holly Ober
Fountain: UCLA
Contact: Holly Ober – UCLA
Image: Image is credited to Neuroscience News.
Original research: Open access.
“Feeding control via a bottom-up subthalamic midbrain pathway.” by Avishek Adhikari, et al. Nature Communications
Abstract
Feeding control via a bottom-up subthalamic midbrain pathway.
The investigative exploration and foraging that lead to food consumption are vitally important but are not well understood. Since GABAergic inputs to the lateral and ventrolateral periaqueductal gray (l/vlPAG) control such behaviors, we analyzed the role of vgat-expressing GABAergic l/vlPAG cells in exploration, foraging, and hunting.
Here, we show that in mice vgat l/vlPAG cells encode food access and consumption of both live prey and non-prey foods. The activity of these cells is necessary and sufficient to induce the search for food and its subsequent consumption.
Activation of vgat l/vlPAG cells produces exploratory foraging and compulsive eating without altering defensive behaviors. Furthermore, l/vlPAG vgat cells are bidirectionally interconnected to various feeding, exploring, and research nodes, including the zona incerta. Surprisingly, the vgat l/vlPAG projection to the zona incerta bidirectionally controls the approach toward food leading to consumption.
These data indicate that the PAG is not only an ultimate goal of top-down exploration and foraging-related inputs, but also influences these behaviors through a bottom-up pathway.