PsyCh Journal · 2015 · 27 citations · 50 references
Life SciencesNeurobiologyNeuroscienceInflammationNeuroimmunologyPsychoneuroimmunologyCytokine BiologyCytokine-mediated PathologyInflammatory SignalingNeuroinflammationPsychological StressStress-immune InteractionsAnimal Disease ModelsChronic StressImmune Cell ActivationInflammatory Mechanisms In DepressionInflammatory Response To StressNeurobiology Of DepressionNeuroinflammatory Cytokine ResponsesNeuroinflammatory Cytokines
Although proinflammatory cytokine changes in depression have been studied widely, few investigations have searched for specific and common changes in cytokines. In the present study, two animal models of depression were compared: a chronic stress model using forced swim stress and an immune activation model using repeated central lipopolysaccharide (LPS) infusion. The levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 mRNA were examined in the brain regions of the prefrontal cortex, amygdala, and hippocampus using real-time polymerase chain reaction (RT-PCR). It was found that both chronic swim stress and repeated central LPS infusion induced depressive-like behaviors, including decreased body weight, reduced saccharin preference, and increased immobility time or shortened latency of immobility in the tail suspension test. Central TNF-α mRNA expression was elevated in both models and central IL-6 mRNA expression was unchanged in both models. Central IL-1β mRNA expression was increased only in the chronic immune activation model. The findings from this study suggest that TNF-α may be a common risk factor for inflammation in depressive disorders.
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