Scientists discover neural circuit responsible for appetite suppression
Using genetic engineering, scientists at the University of Washington have identified a population of neurons that tell the brain to shut off appetite.
The study, published on 13 October 2013 in the journal Nature, considered what might make an animal lose its appetite. Researchers said there are a number of natural reasons, including infection, nausea, pain or simply having eaten too much.
Nerves within the gut that are distressed or insulated send information to the brain through the vagus nerve. Appetite is suppressed when these messages activate specific neurons – ones that contain calcitonin gene-related peptide (CGRP) in a region of the brain called parabrachial nucleus.
In mouse trials, the researchers used genetic techniques and viruses to introduce light-activatable proteins into CGRP neurons. Activation of these proteins excites the cells to transmit chemical signals to other regions of the brain. When they activated the CGRP neurons with a laser, the hungry mice immediately lost their appetite and walked away from their liquid diet; when the laser turned off, the mice resumed drinking the liquid diet.
“These results demonstrate that activation of the CGRP-expressing neurons regulates appetite,” said Richard Palmiter, Professor of Biochemistry at the University of Washington and Investigator of the Howard Hughes Medical Institute. “This is a nice example of how the brain responds to unfavourable conditions in the body, such as nausea caused by food poisoning,” he said.
Using a similar approach, neurons in other brain regions have been identified that can stimulate the appetite of mice that are not hungry. Researchers said they hoped to identify the complete neural circuit (wiring diagram) in the brain that regulates feeding behaviour. By identifying these neural circuits, researchers said scientists may be able to design therapies that promote or decrease appetite.
The study was conducted by Matthew E. Carter in Richard Palmiter’s laboratory and Marta E. Soden in Larry S. Zweifel’s (Assistant Professor of Pharmacology at the University of Washington) laboratory. Funding for the research was provided by the Davis Foundation, the Klarman Family Foundation, the Howard Hughes Institute and the National Institutes of Health.