These findings are supported by our data that: (i) transient global cerebral ischemia significantly decreased fractalkine/CX3CR1 signaling in the hippocampus; (ii) inhibition of CX3CR1 function exacerbates the ischemia-induced chronic increased in microglial activation and pro-inflammatory cytokine levels; (iii) inhibition of CX3CR1 function worsens ischemia-induced chronic cognitive impairment; and (iv) inhibition of CX3CR1 function in sham rats resulted in increased IL-1β expression and impaired behavioral performance. This evidence concerns the gene CX3CR1 and ischemia.