Exposure to certain types of stressors, but not other, increases the levels of cytokines such as interleukin-1 (IL-1) in the periphery and brain (Grippo et al., 2005; Deak et al., 2005). Increased levels of IL-1 can further sensitize HPA axis responses to subsequent stressor exposures (Schmidt et al., 2003; Johnson et al., 2004). Interleukin-1 (IL-1) is a pro-inflammatory cytokine which is a member of a family of immune factors that communicate inflammation to the central nervous system. IL-1 works to stimulate glucocorticoid release by the adrenal glands (Bernton et al., 1987). This pathway raises the possibility that under certain conditions, stress may inhibit adult neurogenesis by stimulated glucocorticoid release through elevated IL-1. Inflammation, a condition associated with increased IL-1, has been shown to reduce cell proliferation and survival of new neurons in the dentate gyrus of the adult rat (Ekdahl et al., 2003). Administration of IL-1β itself decreases cell proliferation and differentiation of new neurons in the adult mouse dentate gyrus (Goshen et al., 2008; Koo & Duman, 2008). In vivo and in vitro studies suggest that progenitor cells in
