Access to palatable food alters gastrin-releasing peptide and dopamine signalling in the medial prefrontal cortex of adult rats exposed to juvenile stress

Eliza AliE. Ali, J.C. MacKay, M.-C. Audet, J.S. James, C. Cayer, P. Kent, Z. Merali

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Stress-exposure during juvenility increases the susceptibility for anxiety and depressive characteristics in adulthood and is also thought to contribute to the growing prevalence of obesity in school-aged children. Stress can increase food intake and a preference for highly caloric palatable food (PF), contributing to weight gain and a risk of developing obesity while PF has stress-buffering characteristics shown in humans and rodents. A feeding peptide called gastrin-releasing peptide (GRP) is involved in stress response and also reduces feeding. GRP receptors (GRPR) are expressed in the medial prefrontal cortex (mPFC), an area implicated in stress and motivated behaviour. Dopamine receptors 1 and 2 (DRD1 and DRD2) are expressed in the mPFC and are involved in reward, motivation and stress. The aim of the study is to reveal the long-term effect of juvenile stress and access to PF on behavioural and metabolic measures and GRP, GRPR, DRD1 and DRD2 mRNA expression in the mPFC. Male Wistar rats that underwent episodic stressor exposure on postnatal days (PD) 27-29 displayed social anxiety that was reversed by consumption of PF. In contrast to the stress buffering effect, PF in combination with previous stressor exposure led to increased weight gain and accumulation of body fat at PD 60. Qualitative polymerase chain reaction revealed an increase of GRP mRNA expression and no change in GRPR expression in juvenile stressed rats with access to PF. The same group also revealed an increase in DRD2 mRNA expression, whereas DRD1 expression was decreased in juvenile stressed rats irrespective of diet. In conclusion, PF mitigates the effects of juvenile stress in adulthood at the expense of increased adiposity in part due to a dysregulation of GRP and dopamine signaling.