• Inflammation;
  • Brain injury;
  • Lipopolysaccharide;
  • Seizures;
  • Hippocampus;
  • Rat

Summary:  We examined the hypothesis that the introduction of an inflammatory agent would augment status epilepticus (SE)-induced neuronal injury in the developing rat brain in the absence of an increase in body temperature. Postnatal day 7 (P7) and P14 rat pups were injected with an exogenous provocative agent of inflammation, lipopolysaccharide (LPS), 2 h prior to limbic SE induced by either lithium-pilocarpine (LiPC) or kainic acid. Core temperature was recorded during the SE and neuronal injury was assessed 24 h later using profile cell counts in defined areas of the hippocampus. While LPS by itself did not produce any discernible cell injury at either age, it exacerbated hippocampal damage induced by seizures. In the LiPC model, this effect was highly selective for the CA1 subfield, and there was no concomitant rise in body temperature. Our findings show that inflammation increases the vulnerability of immature hippocampus to seizure-induced neuronal injury and suggest that inflammation might be an important factor aggravating the long-term outcomes of seizures occurring early in life.