LPS-induced systemic neonatal inflammation: blockage of P2X7R by BBG on neonatal phase decreases oxidative stress in hippocampus of adult rats

The neonatal period is marked by intense maturation of the immune and central nervous systems and the exposure to inflammation during this phase of life may produce long-term effects on the neural system. Here, we examined the impact of neonatal lipopolysaccharide (LPS) exposure on anxiety and pain sensitivity, as well as the superoxide production in adult rats. We also assessed if the blockage of the P2X7R by its antagonist BBG could modulate the effects of LPS on the central nervous system. Wistar male rats were injected with saline (0.9% solution), LPS (1mg/kg, Escherichia coli) or LPS and BBG (50mg/Kg) on postnatal days (PNDs) 1, 3, 5 and 7. Anxiety was evaluated in the Elevated Plus Maze test and nociception in the Hot Plate and Tail Flick tests during adulthood at PNDs 80, 82 and 84 respectively. At PND89, euthanasia was performed and the brain collected for measuring superoxide levels by Dihydroethidium (DHE). No statistical differences were found in Elevated plus maze, Hot-plate nor Tail-flick tests. However, the persistent systemic neonatal inflammation lead to a higher production of superoxide anion in the hippocampus and the blockage of the P2X7R decreased its production (p