Abstract
Although animal models of depression are produced by loading chronic stress, inducing neuroinflammation, or administering drugs that induce depression, the results obtained in these models have poor reproducibility. Therefore, it is necessary to develop animal models that exhibit definitive symptoms of depression for studies on potential therapeutics. This study aimed to investigate depressive symptoms and their pathogenesis in lipopolysaccharide (LPS)-inflamed mice treated with dexamethasone (DEX). Male ICR mice were injected with LPS, followed by injection with DEX at day later once daily for 6 days. Mice in the LPS+DEX group had significantly longer immobility time in the tail-suspension and forced swim tests than did those in the LPS or DEX only and control groups at 7 days post-LPS administration. In immunohistochemical analysis, significantly lower number of the immature neuronal marker doublecortin-positive cells were observed in the hippocampal dentate gyrus of mice in the LPS+DEX group compared with those of mice in the LPS or DEX only and control groups at 7 days after LPS administration. These results suggest that repeated DEX administration to LPS-inflamed mice may induce definitive symptoms of depression by decreasing the number of immature neurons in the hippocampal dentate gyrus.
