A group of neurons in the amygdala - a brain region involved in regulating emotion and feeding behavior - have been identified that suppress food consumption in mice. The findings, published online this week in Nature Neuroscience, may be relevant for the treatment of eating disorders.
When the energy demands in animals are high, various metabolic signals converge in the brain to trigger a feeling of hunger. Some neurons in a region of the brain called the hypothalamus become more active in response to hunger signals, which triggers a sequence of behaviors that increases food consumption. Little is known, however, about the mechanisms that regulate the cessation of food intake and prevent over eating.
David Anderson and colleagues found that in mice, a subpopulation of neurons in the amygdala were more active after the mice had a meal or consumed quinine, a bitter substance known to suppress appetite. These neurons were characterized by their expression of a protein called PKCdelta. The authors found that artificially increasing the activity of this population of neurons inhibited feeding, whereas artificially silencing these neurons increased food intake. Moreover, they found that these PKCdelta-expressing neurons are connected to several other brain regions known to activate by agents suppressing appetite and food consumption. This suggests that these neurons represent a central node in the system that controls feeding suppression.