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The neurons that make us feel hangry

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Maybe it starts with low energy. Or maybe you’re a little grumpy. You may get a headache or have trouble concentrating. Your brain is sending you the message, “I’m hungry.” find food.

Studies in mice have identified a group of cells called AgRP neurons near the bottom of the brain that can trigger this nasty hunger sensation. Even the feeling of “I’m hungry”. They are located near the brain’s blood supply and have access to hormones coming from the stomach and adipose tissue that indicate energy levels. When energy is in short supply, it acts on various other brain areas to promote feeding.

By eavesdropping on AgRP neurons in mice, scientists can learn how these cells switch on and prompt animals to seek food when nutrients are scarce, and how they sense. began to unravel. food reaches the intestine to turn it back off. The researchers also found that AgRP neurons had abnormal activity in mice that mimic anorexia, and that activating these neurons could restore normal eating patterns in those animals. also found.

Understanding and manipulating AgRP neurons may lead to new treatments for both anorexia and bulimia. “If we can control this hunger, we may be able to better control our diet,” says Amber Alhadev, a neuroscientist at the Monell Chemosensory Center in Philadelphia.

to eat or not to eat

AgRP neurons appear to play an important role in appetite.When AgRP neurons were inactivated in adult mice, the animals stop eating — maybe starve to death. Conversely, when the researchers activated the neurons, the mice jumped into the food dish and devouring yourself.

Experiments conducted in several labs in 2015 helped explain how AgRP neurons work.The researchers found that when mice were not getting enough food, AgRP neurons get fired more often. But for food, especially goodies like peanut butter and Hershey’s Kiss, the look and smell were enough. weaken this activity, within seconds. From this, scientists concluded that AgRP neurons are responsible for seeking food in animals. When the bait is found, it ceases to fire violently.

A research team led by neuroscientist Scott Sternson at the Janelia Research Campus in Ashburn, Virginia, also showed that AgRP neuron activity: make a rat sick. To demonstrate this, the scientists engineered mice such that AgRP neurons began firing when the brain was illuminated by optical fibers (the fibers were still able to move the mice around freely). ). They put these genetically engineered mice in boxes with two different regions. One was black with a plastic grid floor and the other was white with a soft tissue paper floor. When the researchers activated AgRP neurons every time the mice entered one of the two regions, the mice avoided that region.

Sternson, now at the University of California, San Diego, concluded that AgRP activation felt “mildly uncomfortable.” That’s natural in nature, he says. Whenever a rat leaves its nest, it is in danger of predators, and must overcome this fear in order to find and eat food. “These AgRP neurons in him are sort of a driving force that, in a dangerous environment, tries to get out in search of food to stay alive.”

Sternson’s 2015 study found that the sight and smell of food quiet AgRP neurons, but only temporarily, and if the mice were unable to follow the treats, activity quickly returned. showed that. Through additional experiments, Alhadeff et al. found that a more reliable way to turn off AgRP neurons was to: calories reaching the intestine.

The mouse sleeping in this video is engineered to activate AgRP neurons when blue light hits the brain. The mouse is resting after a night of heavy eating. When the researchers turned on the blue light, the mice woke up despite being full and started eating more.
Credits: Daniel Kruger / Michael Crassus

First, Alhadev’s team gave the mice a calorie-free treat—an artificially sweetened gel. As expected, AgRP neuron activity decreased when mice ate the gel, but it was transient. AgRP neurons responded less with each bite as they learned that the snack was not nutritious. Thus, when animals learn whether a treat is truly nourishing, their neurons adjust their hunger dials accordingly.

The team then used a catheter implanted in the abdomen to send calories directly to the stomach in the form of an energy drink, Ensure. This avoided sensory cues that food was coming. And, as a result, the decline in AgRP activity was even longer. In other words, it was the nutrients in the food that blocked AgRP neurons long after eating, Alhadev concluded.

Al-Hadef has since Messages sent by the stomach to AgRP neurons, found to be dependent on nutrients. Intestinal fat triggers signals through the vagus nerve, which travels from the digestive tract to the brain. The monosaccharide glucose sends signals to the brain through nerves in the spinal cord.

Her team is currently investigating why these multiple paths exist. She hopes that a better understanding of how AgRP neurons drive food seeking will ultimately help scientists find ways to keep people from gaining unhealthy weight. I hope Scientists and dieters have sought such treatments, for over a century, it has been difficult to identify simple, safe and effective treatments.of Newest class weight loss drugDrugs such as Wegovy partially act on AgRP neurons, but have unpleasant side effects such as nausea and diarrhea.

Therapies that target only AgRP neurons are likely not to completely solve the weight problem because the need for food is just one component of appetite control, consider the main treatments. Mr. Sternson said. appetite controller in the physiology annual review other brain regions that sense satiety and Make high-calorie foods fun also plays an important role, he says. For example, that’s why you end your Thanksgiving meal with a slice of pumpkin pie, even though you’re full on turkey and mashed potatoes.

Three different nervous systems control hunger and food intake. When the body runs out of energy, AgRP neurons are activated, causing discomfort and an animal to seek food. Food also produces positive emotions regardless of the body’s energetic state, and maintains the desire to eat even when the body is not in an energy deficit. And the satiety and nausea signals tell the brain that the animal isn’t hungry and stop eating.

overcome anorexia

The flip side of overeating anorexia, and even there, researchers believe that investigating AgRP neurons could lead to new therapeutic strategies. People with anorexia avoid food to the point of dangerous weight loss. “Eating food actually makes you feel disgusted,” says Ames Sutton-Hickey, a neuroscientist at Temple University in Philadelphia. There is no specific medicine for anorexia. Treatment may include psychotherapy, general medications such as antidepressants, and, in the most severe cases, force-feeding with a nasal tube. People with anorexia are often restless and hyperactive and may exercise excessively.

Researchers can study this condition using a mouse model of the disease known as anorexia nervosa (ABA). When scientists limit the food given to mice and give them a running wheel to run on, some mice develop an anorexic-like state where they eat less than they are given and usually start running on wheels even during the daytime when mice are inactive. . “What happens to these animals is amazing toxicity,” says neuroscientist Tamas Horvath of the Yale School of Medicine. “They basically get excited by not eating and exercising.”

It’s not a perfect model for anorexia. Perhaps mice aren’t under social pressure to be lean like humans are. Conversely, people with anorexia usually have unrestricted access to food. But this is one of the best imitations of anorexia, says Alhadev. “I think this is as good as it can get.”

To investigate how AgRP neurons are involved in anorexia, Sutton-Hickey carefully monitored food intake in ABA mice. She compared them to mice that were on a restricted diet but had locked exercise wheels and had not developed ABA. She found that ABA mice ate less than other mice. And when they ate, their AgRP activity did not decline as much as after filling their tummies.there was something The wrong way neurons respond to hunger and food cues.

Sutton-Hickey also realized that researchers could solve the problem by engineering ABA mice to activate AgRP neurons when injected with certain chemicals. When these mice were treated with chemicals, they ate more meals and gained weight. “This speaks volumes to the importance of these neurons,” says Horvath, who was not involved in the study. “This shows that these neurons are the good guys, not the bad guys.”

Professor Sutton-Hickey says the next step is to figure out why AgRP neurons respond abnormally in ABA mice. She hopes that there may be important molecules targeted by drugs that help people with anorexia.

Overall, the study of AgRP neurons has given scientists a better understanding of why we eat when we eat. It also provides new clues about drugs that could possibly help people change their eating disorders, whether they take too much or too little. , into healthy habits.


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