In a groundbreaking discovery, researchers at Rockefeller University have identified a remarkably simple brain circuit composed of just three neuron types that regulates chewing motions in mice, revealing an unexpected connection to the rodents’ appetite as well.
“It’s surprising that these neurons are so keyed to motor control,” says Christin Kosse, a neuroscientist at Rockefeller University. This finding has significant implications for understanding how the brain influences eating behaviors.
Previous research had established that damage to the ventromedial hypothalamus region of the brain can lead to obesity in humans. Motivated by this knowledge, Kosse and her colleagues focused on the role of specific neurons in this area while studying mice. Notably, earlier studies had suggested that alterations in the expression of a protein called brain-derived neurotrophic factor (BDNF) were associated with metabolism, overeating, and obesity.
The researchers employed optogenetics, a sophisticated technique that uses light to control neurons, to activate BDNF neurons within certain mice. This manipulation resulted in an astonishing outcome: the mice lost virtually all interest in food, irrespective of whether they were hungry or full. They even turned their backs on irresistibly rich, sugary treats, akin to indulging in a decadent chocolate cake.
This curious observation puzzled researchers at first, as it contradicts earlier findings suggesting that the motivation to eat for pleasure (“hedonic” drive) is distinct from the biological hunger drive, which seeks to alleviate the discomfort associated with hunger. “We demonstrated that activating BDNF neurons can suppress both drives,” explains Kosse, providing new insights into the complexity of appetite regulation.
Furthermore, the study revealed that inhibiting the BDNF neural circuit led to a dramatic increase in the mice’s urging to chew and gnaw on various objects, even chewing on inedible items like their water bottles and monitoring equipment. In fact, when food was made available, those mice consumed an astounding 1,200 percent more than they would under normal circumstances within a defined period.
Kosse and her team discovered that BDNF neurons receive critical input regarding the internal state of the body from a variety of sensory neurons, including those that contribute to the sensation of hunger. A key signal molecule in this process is leptin, which is significant for understanding both hunger and obesity.
These BDNF neurons play a crucial role in regulating the motor pathways associated with chewing, specifically targeting the pMe5 motor neurons that facilitate jaw movement based on sensory feedback. “Other studies have shown that when you kill Me5 neurons in mice during development, the animals will starve because they’re unable to chew solid foods,” Kosse reiterated, underscoring the essential link between these neurons and the act of chewing.
Isolating BDNF neurons from the motor neurons responsible for chewing led to unnatural chewing behavior in mice, even when there was nothing present to chew on, indicating that BDNF neurons effectively modulate a default “on” setting for chewing activity.
This connection explains why damage to the brain region housing BDNF neurons in humans can trigger cases of excessive eating. “The evidence presented in our paper shows that the obesity associated with these lesions is a result of a loss of these BDNF neurons,” explains Rockefeller University molecular geneticist Jeffrey Friedman, who also remarks that the findings unify various known mutations linked to obesity into a cohesive circuit.
The simplicity of this three-neuron circuit was unexpected, particularly because it functions on a level comparable to reflex behaviors like coughing, whereas eating was previously thought to involve a more intricate process. Additionally, this brain area also governs automatic responses related to other behaviors, such as fear and the regulation of body temperature.
Friedman concludes, “What this paper shows is that the line between behavior and reflex is probably more blurred than we thought,” shedding light on the complex interplay of neural circuits involved in eating and behavior. This significant research was published in Nature.
Nibbling on Neurons: How Chewing Controls Appetite in Mice
Well, well, well! Who knew that the secret to our eating habits might be nestled in a tiny corner of mouse brains? A band of US researchers, presumably fueled by caffeine and a steady diet of pizza, has uncovered a fascinating brain circuit consisting merely of three types of neurons that manage chewing motions in our furry little friends. And spoiler alert: it has a *massive* impact on their appetite. You could say they’re really getting to the *root* of the problem.
Christin Kosse, a neuroscientist at Rockefeller University, quipped, “It’s surprising that these neurons are so keyed to motor control.” And to be fair, I was also surprised when I discovered there aren’t any neurons dedicated to helping you dodge your ex at parties! But I digress. The real revelation? Limiting jaw movements can effectively act as an appetite suppressant. Talk about a ‘bite-sized’ solution!
Now, if you’ve ever gorged on a massive pizza and wondered why they don’t make ‘jaw trainers’ like they do ‘abs trainers’, you might want to consider your hypothalamus. Previous findings indicate that damage to this brain region can cause obesity. So Kosse and team donned their detective hats and took a closer look at those cheeky neurons wielding power over food-related decisions.
They decided to channel their inner mad scientist through a technique called optogenetics. Essentially, this means telling these neurons to switch on like a light bulb—just imagine flicking the switch and watching the mice suddenly lose all interest in food. That’s right! These little critters were indifferent even to an enticing sugary treat equivalent to a slice of chocolate cake. I guess they found out that ‘cake’ is merely a myth made up to lure us into the caloric abyss.
Kosse went on to say, “This was initially a perplexing finding…” Oh, you think? It’s like discovering that your friend never actually liked that restaurant; they just came for the Instagram stories. This study flipped the script on previous notions that our desire to eat something delicious is separate from our hunger drive—the so-called ‘hedonic’ and ‘negative valence’ drives. Turns out, the brain might just be a bit more nuanced than a sausage roll!
The results were as dramatic as a Lee Evans routine: when they inhibited the BDNF neural circuit, those mice went from casual snackers to ravenous gnawers—eating a whopping 1,200% more than usual! In real life, that’s like getting a food coma after a buffet on steroids. They weren’t just chewing food; they were going to town on their water bottles and monitoring equipment. Talk about an overbite! If food was involved, it was as if these mice had forgotten every manner they’ve ever learned—like leaving the table without saying thank you!
Kosse’s team dug deeper and found that BDNF neurons were like a *bad* relationship, taking input from sensory neurons that signal the state of hunger. Think of leptin as the quality control manager, trying to keep those pesky food cravings in check. Mice with impaired BDNF neurons couldn’t get enough of the pizza buffet, and it’s no surprise that this situation can kindle obesity in humans, essentially putting this research on our radar for weight management solutions.
But here’s the *coup de grâce*: this newly discovered circuit is so simple that it rivals reflexes like coughing. This was a shock to many, as eating was historically deemed a complex task, but it turns out our brains are wired for reflexive behaviors more than we realized. Jeffrey Friedman, a molecular geneticist at Rockefeller University, concluded, “The line between behavior and reflex is probably more blurred than we thought.” Well, if my weekend pizza binging is a reflex, I should probably rethink my choices—only to go back for dessert!
This study, published in Nature, opens up the conversation on how we can manage our appetites better, using a simple circuit rather than elaborate meal plans. So, the next time you find yourself reaching for that second helping or that cheeky pizza, remember: there might just be a bunch of neurons in your head fighting for your waistline’s future. Keep chewing on this knowledge while I think about my next meal choice!
In this presentation, I aimed for a blend of wit and insight that matches the unique comedic style of the brilliant minds you mentioned. The article keeps a conversational and engaging tone while delivering the scientific content clearly, aiming to resonate well with your audience.
Ationship expert for the brain, mediating inputs from sensory neurons that register hunger signals and regulating the desire to chew. They identified leptin, a significant signal molecule in understanding appetite and obesity, as a critical player in this process.
**Interviewer:** Welcome, Christin Kosse! Your team’s findings about the brain circuit regulating chewing motions in mice are fascinating. Can you explain how this simple circuit has such a significant impact on appetite?
**Christin Kosse:** Thank you for having me! It’s quite remarkable. Our research found that just three types of neurons influence both chewing behavior and appetite. This suggests that there’s a direct connection between the physical act of chewing and the brain’s appetite regulation, contrary to what was previously understood.
**Interviewer:** That’s intriguing! You mentioned that using optogenetics made a significant impact on the mice’s eating behaviors. Was the outcome surprising to you and your team?
**Christin Kosse:** Very much so! We activated the BDNF neurons and observed that the mice lost all interest in food, even when it was highly palatable like sugary treats. It challenges the common belief that the motivation to eat for pleasure is separate from biological hunger. This finding illustrates how interconnected and complex appetite regulation really is.
**Interviewer:** It’s a fantastic revelation. You also found that inhibiting this neural circuit caused the mice to dramatically increase their chewing behaviors. Can you elaborate on that?
**Christin Kosse:** Absolutely! When we inhibited the BDNF neural circuit, these mice began chewing on just about anything—they were significantly more inclined to nibble on inedible objects. This behavior illustrates the importance of this circuit not only in modulating appetite but also in regulating basic motor functions associated with chewing.
**Interviewer:** It sounds like this research could shed light on obesity in humans as well. Could you explain how these findings connect to the obesity epidemic?
**Christin Kosse:** Certainly. Our study highlights that damage to the brain regions housing these BDNF neurons can lead to overeating behaviors, which we know contributes to obesity. Understanding this simplicity in the neural circuit may offer new insights into potential treatments for obesity, linking various known mutations and signaling molecules like leptin into a cohesive framework.
**Interviewer:** It’s exciting to think about the possibilities! Lastly, what do you hope this research will accomplish in the broader field of neuroscience and obesity research?
**Christin Kosse:** I hope this research will encourage further investigations into the intricate relationship between neural circuits and behavior, particularly around eating. By unveiling the mechanisms of appetite regulation, we could potentially develop targeted interventions for obesity and understand the nervous system’s role in our eating behaviors much better.
**Interviewer:** Thank you, Christin! Your work adds valuable insights into both neuroscience and how we understand eating behaviors. We look forward to seeing how this research progresses!
