Cells found in mouse brain that signal stop eatingAmy Walsh (Author) Published Date : Mar 18, 2016 20:35 IST
Scientists at Johns Hopkins say they have found a new type of nerve cell that seems to control feeding behaviors in mice. The finding, they report, adds significant detail to the way brains tell animals when to stop eating and, if confirmed in humans, could lead to new tools for fighting obesity. Details of the study will be published by the journal Science.
When the type of brain cell we discovered fires and sends off signals, our laboratory mice stop eating soon after, says Richard Huganir, Ph.D., director of the Department of Neuroscience at the Johns Hopkins University School of Medicine. The signals seem to tell the mice they've had enough.
Huganir says his team's discovery grew out of studies of the proteins that strengthen and weaken the intersections, or synapses, between brain cells. These are an important target of research because synapse strength, particularly among cells in the hippocampus and cortex of the brain, is important in learning and memory.
In a search for details about synapse strength, Huganir and graduate student Olof Lagerl f, M.D., focused on the enzyme OGT -- a biological catalyst involved in many bodily functions, including insulin use and sugar chemistry. The enzyme's job is to add a molecule called N-acetylglucosamine (GlcNAc), a derivative of glucose, to proteins, a phenomenon first discovered in 1984 by Gerald Hart, Ph.D., director of the Johns Hopkins University School of Medicine's Department of Biological Chemistry and co-leader of the current study. By adding GlcNAc molecules, OGT alters the proteins' behavior.
To learn about OGT's role in the brain, Lagerl f deleted the gene that codes for it from the primary nerve cells of the hippocampus and cortex in adult mice. Even before he looked directly at the impact of the deletion in the rodents' brains, Lagerl f reports, he noticed that the mice doubled in weight in just three weeks. It turned out that fat buildup, not muscle mass, was responsible.
When the team monitored the feeding patterns of the mice, they found that those missing OGT ate the same number of meals -- on average, 18 a day -- as their normal littermates but tarried over the food longer and ate more calories at each meal. When their food intake was restricted to that of a normal lab diet, they no longer gained extra weight, suggesting that the absence of OGT interfered with the animals' ability to sense when they were full.
These mice don't understand that they've had enough food, so they keep eating, says Lagerl f.
That result suggests that, in these cells, OGT helps maintain synapses, says Huganir. The number of synapses on these cells was so low that they probably aren't receiving enough input to fire. In turn, that suggests that these cells are responsible for sending the message to stop eating.
There are still many things about this system that we don't know, says Lagerl f, but we think that glucose works with OGT in these cells to control 'portion size' for the mice. We believe we have found a new receiver of information that directly affects brain activity and feeding behavior, and if our findings bear out in other animals, including people, they may advance the search for drugs or other means of controlling appetites.
Cells found in mouse brain that signal stop eating