The need to eat is one of the most primal instincts we have as humans and one that connects us, evolutionarily, to almost all organisms. Yet, the exact cellular mechanisms that regulate this primordial pathway has alluded researchers for many years. However now, investigators at the University of Arizona (UA) believe they have identified a brain region that regulates appetite suppression and activation. Curiously, this neuronal center is tucked within the amygdala, the brain’s emotional hub. Findings from the new study were published recently in Nature Communications through an article titled, “A bed nucleus of stria terminalis microcircuit regulating inflammation-associated modulation of feeding.”

Interestingly, the UA research team uncovered the neurocircuitry while they were studying mechanisms that control extreme appetite loss, called anorexia. Anorexia can be triggered by disease-induced inflammation and can negatively impact recovery and treatment success. It is harmful to the quality of life and increases morbidity in many diseases, the researchers noted.

“By silencing the neurons within the circuit, we can effectively block feeding suppression caused by inflammation to make patients eat more,” explained senior study investigator Haijiang Cai, PhD, assistant professor, and BIO5 research fellow. “We used anorexia for simplification, but for people with obesity, we can activate those neurons to help them eat less. That’s the potential impact of this kind of study.”

To determine if the specific neurons within the amygdala control feeding behavior, the UA research team inhibited the neurons, which increased appetite. They then activated the neurons, causing a decrease in appetite.

“We identified a population of neurons, marked by the expression of protein kinase C-delta, in the oval region of the bed nucleus of the stria terminalis (BNST), which are activated by various inflammatory signals,” the authors wrote. “Silencing of these neurons attenuates the anorexia caused by these inflammatory signals. Our results demonstrate that these neurons mediate bidirectional control of general feeding behaviors. These neurons inhibit the lateral hypothalamus-projecting neurons in the ventrolateral part of BNST to regulate feeding, receive inputs from the canonical feeding regions of the arcuate nucleus and parabrachial nucleus.”

While feeding may sound simple, it’s not, Cai commented. People feel hunger either to satisfy nutritional deficits or for the reward of eating something good. Once the food is found, we check that it’s good before chewing and swallowing. After a certain point, we feel satisfied. Theoretically, each step is controlled by different neurocircuitry.

“This circuitry we found is really exciting because it suggests that many different parts of brain regions talk to each other,” Cai said. “We can hopefully find a way to understand how these different steps of feeding are coordinated.”

The brain region was found in mouse models and the next step is to identify a homologous area in humans, in order to validate if those same mechanisms exist. If they do, then scientists might be able to find some way of controlling feeding activities.

“Our data define a BNST microcircuit that might coordinate canonical feeding centers to regulate food intake, which could offer therapeutic targets for feeding-related diseases such as anorexia and obesity,” the authors concluded.

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