Binge Eating Disorder is an Eating Disorders characterized by eating a large amount of food in a discrete period of time in absence of physical hunger.
Subjects suffering from this pathology exhibit lack of control, impulsivity and compulsivity traits that recall the "behavioral addiction" that characterizes and defines the substance use disorders.
Clinical and preclinical studies indicate the cortico-accumbal catecholaminergic circuit as a common substrate for pathological responses to drug and food and new insights highlight a critical role for serotoninergic system in modulating this circuit as well as the motivated behavior.
Due to ethic and technical limitations in human studies, this field of neuroscientific research needs preclinical models to disentangle the role of constitutive and environmental elements in etiopathology and clinical course.
We have recently proposed a mouse model evidencing how adult response to both natural and pharmacological rewarding stimuli is enhanced by exposure to early unstable environment (Repeated Cross Fostering - RCF) in C57 inbred strain of mouse. Analysis of neurobiological substrates has evidenced profound alterations in cortico-accumbal dopaminergic system functionality.
In this project, using an animal model, we aim to investigate the serotoninergic-dopaminergic interplay within this circuit in mediating susceptibility to develop a binge eating-like phenotype.
Behavioral and neurochemical analysis of constitutive differences between susceptible (RCF) and Control mice as well as alterations induced in these different groups by a binge-inducing dieting, will increase the comprehension of binge eating disorder possibly identifying early risk-predictors and proposing new targeted and more effective pharmacological therapies in humans.
The proposed project is placed within an innovative research field, employing interdisciplinary knowledge and methods and innovative technologies to achieve results of high translational impact and scientific value.
Neurobiological basis of Binge Eating Disorder is not fully investigated and the role of 5HT-DA system interplay in susceptibility and resilience to binge eating disorder remains largely unknown. Here we propose to examine the critical role for cortical 5HT1ARs and accumbal 5HT2BRs in mediating the vulnerability to develop binge eating-related behavioral and neurochemical phenotype.
Results from present study will be useful to the development of new therapies for the treatment of Binge Eating Disorders that in turn will reduce both the direct costs associated with prevention and health treatment activities, as well as the indirect costs deriving from collateral activities such as the treatment of secondary pathologies.