1B&1C). The findings of behavioral deficits in CX3CR1-deficient mice support our previous work with older BALB/c mice, in which the exaggerated sickness response after LPS injection [33] was also associated with prolonged depression-like behavior [19]. These findings are relevant because they suggest that a deficit in CX3CR1-mediated regulation of microglia is sufficient to cause prolonged sickness and depression-like behaviors after LPS injection even in the absence of the myriad inflammatory changes associated with aging. This evidence concerns the gene CX3CR1 and depressive disorder.