Every time as you are contemplating the decision of having one more chip a battle is fought in the brain. This is true, but how soon one group gets on top is the critical factor in how soon that bag of chips gets passed back to the vendor.
That is why, at present, researchers have recently identified a new link in this neural network signal that controls hunger and satiation, which is an as yet unknown type of neuron that works as an instant antidote to this desire. The data are published in Nature.
“This new type of neuron alters the way the feeding is controlled at the conceptual level,” explains Han Tan, a research associate in the Rockefeller’s Laboratory of Molecular Genetics led by Jeffrey Friedman.
Traditionally, the brain’s so-called feeding circuit was thought to involve a simple feedback loop between two types of brain cells in the hypothalamus: While a gene named AGRP makes neurons promote hunger and POMC makes neurons promote satiety.
Earlier it was assumed that these two populations were the only two lists that are targeted by leptin, but later such a model was deemed deficient. Activation of AGRP neurons rapidly increases appetitive behaviour, whereas activation of POMC neurons takes several hours to suppress it.
People and the researchers ask themselves if they missed something. “We thought POMC could not counteract these neurons fast enough to inhibit feeding,” Tan adds. And so we asked ourselves whether there was another neuron that could increase the rate of satiety, on the same time scale as AGRP.
This newly identified BNC2 neuron is particularly sensitive to food stimuli and works to quickly suppress hunger. The present study shows that, when BNC2 neurons are engaged by leptin and maybe other signals, they not only dampen appetite but also decrease aversive feelings caused by hunger. Noteworthy, these neurons work as inhibitory signals for AGRP neurons, and they can do it promptly while acting as an opposite signal.
“This has added a new critical layer to the neural circuit that controls appetite and expands on how leptin is inputting into it,” Friedman added. ‘It also addresses a matter regarding feed regulation at different time scales by different neurons.”
Redefining hunger
While BNC2 neurons are important in the treatment of obesity and metabolic disorders the discovery of these neurons has major implications for science in general. “We are considering its potential to be a newfound therapy for obesity and diabetes,” Tan said, referring to a study that identifies a genetic association between BNC2 and high body mass index and diabetes in patients.
The team is also looking into whether activating or inhibiting these neurons influences glucose and insulin, which makes the prospects of this kind of therapy even more appealing. If BNC2 neurons are involved in regulating hunger could there be other neural circuits for other behaviours like grooming or sleeping?
Finding other related circuits might help us expand our knowledge of how the complexity of actions is orchestrated through different instinctual behaviours, and therefore–open quite a few more horizons in behavioural neurology.
“We now consider BNC2 and AGRP as those kinds of foods Yin Yang feeds on,” Tan says.
Reference: Tan HL, Yin L, Tan Y, Ivanov J, Kaja Plucinska, Anoj Ilanges, et al. Leptin-activated hypothalamic BNC2 neurons acutely suppress food intake. Nature
