These neurons affect how much you do, or don’t, want to eat

Summary: Neurons in the bed nucleus of the stria terminalis (BNST) appear to regulate food intake. The neurons appear to form part of a network that controls appetite loss in mice.

Source: University of Arizona

Like a symphony, multiple brain regions work in concert to regulate the need to eat. University of Arizona researchers believe they have identified a symphony conductor – a brain region that regulates appetite suppression and activation – tucked within the amygdala, the brain’s emotional hub.

The UA Department of Neuroscience team found the neurocircuitry controlling appetite loss, called anorexia, said assistant professor Haijiang Cai, who is a member of the BIO5 Institute and heads up the neuroscience lab that ran the study.

Anorexia can be triggered by disease-induced inflammation, and can negatively impact recovery and treatment success. It is harmful to quality of life and increases morbidity in many diseases, the authors wrote. The paper, “A bed nucleus of stria terminalis microcircuit regulating inflammation-associated modulation of feeding,” was published June 24 in Nature Communications.

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

“By silencing the neurons within the circuit, we can effectively block feeding suppression caused by inflammation to make patients eat more,” Cai said.

“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.”

Feeding sounds simple, but it’s not, Cai related. 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.

This shows someone eating pizza

The researchers concluded that NGF is a key driver of the development of IBS following early-life stress. The image is in the public domain.

Theoretically, each step is controlled by different neurociruitry.

“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 mice models. The next step is to identify it in humans and validate that same mechanism exist. If they do, then scientists can find some way to control feeding activities, Cai said.

Cai’s co-authors, all of whom were associated with the Department of Neuroscience during the research, are lead author Yong Wang, JungMin Kim, Matthew B. Schmit, Tiffany S. Cho and Caohui Fang.

Funding: The research was partially funded by the Brain and Behavior Research Foundation.

About this neuroscience research article

Source:
University of Arizona
Media Contacts:
Mikayla Mace – University of Arizona
Image Source:
The image is in the public domain.

Original Research: Open access“A bed nucleus of stria terminalis microcircuit regulating inflammation-associated modulation of feeding”. Yong Wang, JungMin Kim, Matthew B. Schmit, Tiffany S. Cho, Caohui Fang & Haijiang Cai.
Nature Communications. doi:10.1038/s41467-019-10715-x

Abstract

A bed nucleus of stria terminalis microcircuit regulating inflammation-associated modulation of feeding

Loss of appetite or anorexia associated with inflammation impairs quality of life and increases morbidity in many diseases. However, the exact neural mechanism that mediates inflammation-associated anorexia is still poorly understood. Here 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. 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 arcuate nucleus and parabrachial nucleus. Our data therefore 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.

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