One explanation could have been that the mice were anxious or frightened, and so stopped eating. The researchers took a number of steps to rule that out. They also established that this group of neurons was likewise activated by bad tastes and “visceral malaise” — feeling nauseated — both of which caused the mice to stop eating.

The conclusion, Dr. Anderson said, was that this small group of neurons might be an appetite-control hub. These are neurons that inhibit behavior. So when the researchers activated them, appetite was turned off. The researchers were also able to turn appetite on, by stopping the neurons from sending signals. For that they used a different kind of genetic manipulation and a different wavelength of light.

Richard D. Palmiter, a University of Washington neuroscientist who has also studied how the brain controls feeding behavior, said, “I think it’s likely that these neurons in the amygdala help an animal avoid toxic or unpleasant foods.” But there are many other ways the brain regulates appetite and feeding, he added.

Dr. Anderson said that people may well have a similar appetite control network in a similar location, which would be intriguing because the amygdala is so strongly associated with emotion, particularly fear and anxiety. Appetite and emotions are certainly connected, and the chance to find out something about those connections at the level of brain circuits is exciting.

He pointed out that electrical brain stimulation has been tried with some success for people with severe depression, so a comparable intervention might be considered in the case of a life-threatening eating disorder if indeed people have the same kind of appetite control network.

In terms of basic understanding of the brain, Dr. Anderson said, the finding suggested “the incredible specificity of neurons in the brain.” This apparent control hub, he said, is “a subset of neurons in a subdivision of a subdivision of the amygdala,” which itself is only a small part of the brain.