It is well established that stress and negative affect (e.g., sadness, anger) trigger overeating (Stein et al., 2007). This form of maladaptive eating behaviour, commonly referred to as “emotional eating”, is particularly common in women, and is associated with binge eating and higher risk of obesity (Wong et al., 2020). The neural mechanisms that underpin this form of dysregulated eating are yet to be elucidated but likely implicate neuronal substrates involved in both stress and reward. This study aimed to identify brain regions and specific neuronal phenotypes associated with the propensity for stress-induced binge eating in females using a translationally relevant mouse model.
Female Corticotropin Releasing Hormone (CRH)-IRES-Cre x tdTomato reporter mice were divided into stress-binge prone and resistant subgroups based on the extent of binge eating observed in an intermittent access protocol involving exposure to a mild, psychological stressor. Immunohistochemical analyses of coronal brain sections were then performed in order to assess levels of the neuronal activity marker Fos and the neuropeptide oxytocin. Use of the CRH reporter mice in combination with immunolabelling for Fos and oxytocin allowed the identification of differences in recruitment of specific regions between behavioural groups and the neurochemical phenotype of these cells.
Binge prone mice displayed significantly higher binge eating of a palatable food reward compared to both binge resistant mice and a control group consisting of mice that consumed the same food in the absence of prior stress exposure. Quantification of immunohistochemical data is ongoing and will provide insight into the neural correlates which potentially underlie the differential behavioural response to both the food reward and the “emotional” stressor in our stress binge paradigm. Quantification of double and triple labelling of oxytocin and CRH positive cells will reveal whether there is a potential role for these neuropeptides in stress induced binge eating.
Ultimately, individual variation in binge eating displayed by our stress-exposed female mice recapitulates the natural individual differences characteristic of the human, female binge eating continuum. Hence using this model to investigate discrepancies in the recruitment and activation of different regions between prone and resistant groups may facilitate our understanding of the precise neural mechanisms driving this behaviour.