We have previously demonstrated that administration of an IL- 1β antagonist blocks the inhibitory effects of stress on neurogenesis, as well as the expression of depressive behaviors (Koo and Duman, 2008). In addition, IL-1R null mice are resistant to the development of depressive behaviors, including anhedonia, caused by chronic stress exposure (Koo and Duman, 2009). These studies indicate that blockade of IL-1R, or the production and release of IL-1β would produce antidepressant effects. We have also reported that blockade of IL-1R downstream signaling molecules, such as IκK, Iκb, and nuclear factor kappa B (NF-κB), blocks the reduction of neurogenesis caused by stress (Koo and Duman, 2008, 2009; Koo et al., 2010). These findings indicate that inhibitors of IL-1β-signaling could be useful for the treatment of depression.
