Val Charbonneau

  • Master’s Student (Neuroscience)
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For my thesis project, I endeavor to examine the underlying neurobiological and hormonal mechanisms involved in anorexia nervosa (AN), with particular emphasis on the effects of exposure to stressors during the juvenile period on adult metabolism and stress responses. Indeed, stress during adolescence has been linked as a factor that triggers the onset of eating disorders including AN. In our studies, we intend to use a modified version of the resident/intruder paradigm . Pilot studies in our lab have shown that this manipulation causes females (but not males) to become thinner and consume less food than non-stressed controls. Once determined a valid paradigm, we will examine if the hormonal profile of these mice is similar to that of AN women, including high levels of stress and metabolic hormones such as corticosterone and ghrelin, and low leptin and insulin levels. We will also monitor behavioral responses such as hyperactivity, altered circadian (sleep/wake cycles), susceptibility to develop activity based anorexia and altered hypothalamic peptide expression. As a final phase to my project, I will try to determine the contribution of ghrelin to producing the effects of juvenile stress on these females. It is possible that ghrelin responses, an orexigenic peptide, following stress may protect against metabolic challenges, but chronic exposure may lead to ghrelin insensitivity and thus to processes where metabolism and behavior are altered so as to generate a thin phenotype and decreased eating. If so, we would expect that mice lacking ghrelin receptors may be more vulnerable to stress-induced anorexia. These proposed models serve as a possible avenue that will further aid in understanding the physiological basis of AN and eventually contribute to a pharmacological treatment plan to successfully intervene while behavioral and cognitive treatments are taking place.