Microglia are highly motile, phagocytic cells that are capable of releasing various signaling molecules including inflammatory cytokines (e.g. IL-1, TNF-alpha, and IL-6). Recent studies have indicated that stress has profound impacts on microglia morphology, density, proliferation, and activation state, implicating their role in certain pathologies (Tyan et al). Our lab has previously shown that exposure to chronic stress induces anhedonic behavioral responses in Fischer-344 rats after a 4-day chronic mild stress paradigm (Camp et al). To examine the activation state of microglia after this chronic mild stress protocol, microglia were isolated from the hippocampus and placed in culture to measure pro-inflammatory cytokines and their phagocytic capacity. Following 4h in culture basal IL-1, TNF-alpha, and IL-6 protein production were not altered in microglia collected from stressed animals compared to microglia collected from controls. After LPS stimulation IL-1 production was attenuated in microglia collected from stressed animals while there were no changes in the production of TNF-alpha or IL-6. Microglia stimulated with LPS and treated with the highest dose of norepinephrine resulted in an increase in IL-1 production and a decrease in TNF-alpha production in both control and stressed animals. Evidence has implicated that following stress exposure, peripheral monocytes translocate to the brain and have shown to promote anxiety like behavior (Wohleb et al). To look at the affect stress has on peripheral immune cells, phagocytic ability was measured. Trends indicate that norepinephrine inhibits phagocytosis in home cage controlled animals while peripheral immune cells from stressed animals show little response to norepinephrine.