Repeated stress induces emotional changes and cognitive impairments, and is a risk factor for psychiatric disorders. Rodent studies have revealed critical roles of dopaminergic systems and inflammation-related molecules derived from microglia in repeated stress-induced behavioral changes. Acute stress preferentially activates the dopaminergic pathway projecting to the medial prefrontal cortex (mPFC) through glucocorticoid receptor. This dopaminergic activation impairs working memory functions, but suppresses stress-induced social avoidance. Repeated stress attenuates this dopaminergic pathway, and consequently impairs working memory function and promotes stress-induced social avoidance. In contrast, repeated stress increases the excitability of the dopaminergic pathway projecting to the nucleus accumbens (NAc), from which BDNF is released in NAc and promotes stress-induced social avoidance and anhedonia. In addition, repeated stress induces expression of inflammation-related molecules in microglia through beta-adrenergic receptors. Under repeated stress, IL-1 beta induces behavioral depression and anxiety, perhaps partly through suppressing proliferation of neural stem cells in the hippocampus. IL-1 receptor signaling in endothelial cells augments expression of inflammation-related cytokines in microglia, thereby promoting stress-induced behavioral changes. TNF alpha and IL-6 are also critical for stress-induced depression-like behaviors. Repeated stress increases synthesis of prostaglandin (PG) E2 in microglia through PG synthase COX1. PGE2 in turn attenuates the dopaminergic pathway to mPFC through EP1 receptor, thereby promoting social avoidance by repeated stress. These findings show that repeated stress induces behavioral changes through neurotransmitters and inflammation-related molecules as well as the crosstalk between neurons and microglia.