Chronic stress-dependent activation of somatostatin neurons in the nucleus accumbens facilitates maladaptive eating behaviors

Thesis: S.M., Massachusetts Institute of Technology, Department of Brain and Cognitive Sciences, 2016.Cataloged from PDF version of thesis.Includes bibliographical references (pages 24-27).Stressors are known to impact eating behaviors. However, recapitulating the intricate interplay between chronic stress and aberrant human eating patterns in an animal model remains a challenge. Notably, binge eating, a diagnostic feature associated with many types of eating abnormalities, particularly pertains to the binge eating disorder. To more closely investigate the etiology underlying eating behavior-associated maladaptation, the present study provides a novel and ethologically relevant animal model based on predatory odor stress. My data show that chronic stress in female mice selectively increases consumption of highly palatable, but not the regular, diet, when it is presented during a limited time following stress exposure. In addition, the nucleus accumbens (NAc), a key component in the neural circuitry of reward, is also an established neural substrate susceptible to the effects of stress. Given the cellular complexity in NAc, identifying the neuronal subtypes that are selectively involved in chronic stress-elicited physiological and behavioral alterations will provide grounds for further understanding in the underlying cellular changes. Because deficits in the somatostatin (SOM) neurons have been implicated in mice exhibiting traits of anxiety and depression, this neuron subtype may play an important role in modulating negative behavioral emotionality. Here I report an abundance of somatostatin neurons, majority of which are located in the rostral-ventral region of the NAc and are activated by chronic stress exposure. Together, these results provide the first line of evidence in linking chronic stress and the somatostatin neurons within the NAc to binge eating. Further fluorescent labeling quantification and cell-type-specific optogenetic manipulation will be needed to further delineate the role of SOM neurons in orchestrating the inhibitory components of stress-modulated reward circuitry.by Elizabeth Liu.S.M