89. The effect of acute metabolic stress on anhedonia and IL-1 beta expression following chronic stress

Abstract

There is high comorbidity between metabolic syndrome and depression. Here we examine if acute metabolic stressors, either overnight food deprivation or 2-deoxyglucose injection (250 mg/kg), would potentiate anhedonia and IL-1 β expression following chronic mild stress. To test this we measured sucrose preference and IL-1 β in both control and stressed animals with or without a metabolic stressor. Our results found that chronic mild stress induced depressive behaviors in only a portion of the animals (stress-susceptible), while other animals continued to have high levels of sucrose preference that were similar to controls (stress-resistant). Exposure to food deprivation prior to testing did not affect sucrose preference in control animal nor did it alter the reduced sucrose preference in stress-susceptible animals, but overnight food deprivation caused a significant decrease in sucrose preference in stress-resistant animals. 2-Deoxyglucose injection caused a significant reduction in both control and stressed animals’ preference for sucrose. Additionally, there was no effect of chronic stress on IL-1 β levels, but food deprivation caused an increase of IL-1 β in the hippocampus and brainstem; decreased levels in the prefrontal cortex; and a potential interaction between stress and food deprivation in the hypothalamus ( p = 0.10). Our results indicate that metabolic stressors likely interact with psychological stressors to promote depression-like responses and that more severe metabolic stressors may themselves induce anhedonic responses. Furthermore, metabolic stressors affect regional levels of brain cytokines.