Published on September 27, 2013 at 5:12 AM
"We were able to really home in on the precise neural circuit connection that was causing this phenomenon that's been observed for more than 50 years," Stuber said.
The study, which uses technologies highlighted in the new National Institutes of Health Brain Initiative, suggests that faulty wiring in BNST cells could interfere with hunger or satiety cues and contribute to human eating disorders, leading people to eat even when they are full or to avoid food when they are hungry. Further research is needed to determine whether it would be possible to develop drugs that correct a malfunctioning BNST circuit.
"We want to actually observe the normal function of these cell types and how they fire electrical signals when the animals are feeding or hungry," Stuber said. "We want to understand their genetic characteristics - what genes are expressed. For example, if we find cells that become really activated after binge eating, can we look at the gene expression profile to find out what makes those cells unique from other neurons."
And that, Stuber said, could lead to potential targets for drugs to treat certain populations of patients with eating disorders.
UNC School of Medicine neurobiology graduate student Josh Jennings is the first author on Stuber's paper in Science. Authors also include members of his research team, neurobiology grad student Alice Stamatakis, research technician Randall Ung, and Giorgio Rizzo of the University Medical Center Utrecht in the Netherlands.
For this study, Stuber received funding from the National Institute on Drug Abuse and the Klarman Foundation, a private organization that funds basic research related to eating disorders.