Grant: Operating Grant

Nowadays, in our modern lives we are facing everyday stress, but on the other hand, we have easy access to 'comfort' food, highly palatable sweets and desserts. After 'sweet misbehavior' we can try to restore our 'healthy lifestyle' by dieting, but this worsens the situation, and our appetite gets out of the control! This anecdotal example is supported by the huge increase in the prevalence of binge eating disorder and interrelated metabolic problems during the three last decades. But what do we know about the neuronal mechanisms of binge eating? So far the progress in the development of treatment strategies for this pathology is limited because the neurological mechanisms of eating disorders are not clearly understood and cannot be studied easily in humans. Therefore, there is a great need for adequate animal models. We have developed the sucrose-sensitized and sucrose-binge-eating rat models using chronic intermittent access to palatable sucrose and food restriction. These models are characterized by excessive sucrose-licking activity and sucrose binge eating. Sucrose-sensitized and sucrose-binge-eating rats demonstrate attenuated anorectic stress effects and lower neuronal activation in the lateral septum, the forebrain structure expressing the receptors for stress hormones. It seems that the anorectic effects of stress hormones are modulated at the level of the lateral septum by inhibitory mechanisms developed in binge-eating model. The present project will study how the effects of stress hormones are modulated by palatable food, which neuromediators are involved in this modulation, and their neuroanatomical distributions. In addition, we will study how neuronal activity in the lateral septum is altered in freely moving, sucrose-sensitized and sucrose-binge-eating rats. This project will shed light on the neuronal mechanisms related to stress and eating disorders.