CCL2 and injury: Attenuation of inflammation and microglial activation has been shown to confer neuroprotection in neonatal HI brain injury [21], [34], and we have previously demonstrated that increased microglia formation after HI in neonatal and juvenile mice, both in the hippocampus [36] as well as in the cortex and striatum [37], is concurrent with increased expression of the pro-inflammatory markers CCL2 (MCP1) and IL-18 [36], [37].