The relationship between seizures and neuronal injury in experimental animals is influenced by the stage of development and the model employed to produce experimental status epilepticus (SE) (Sankar et al., 1997; Sankar et al., 1998; Sankar et al., 2000; Cilio et al., 2003). In these experimental models, younger animals show a decreased tendency to demonstrate neuronal injury, especially in the CA3 and hilar regions of the hippocampus (Sanker et al., 1997; Sanker et al., 1998; Sankar et al., 2000; Cilio et al., 2003; Haas et al., 2001). However, P14 animals showed a striking level of CA1 injury in the lithium-pilocarpine model of SE. There is an apparent discrepancy between animal models and some clinical situations in terms of the consequences of prolonged seizures in the immature brain. Prolonged febrile seizures have been demonstrated to produce signal changes in the MRI that are consistent with hippocampal injury (VanLandingham et al., 1998). Neuronal injury in neonates who had sustained hypoxic-ischemic was more severe when the encephalopathy was complicated by seizures (Miller et al., 2002). The developmental outcome of neonates with electrographic seizures was worse than that of a cohort without seizures even though the two groups were matched for Apgar scores, initial cord blood pH, and base deficits (McBride et al., 2000). Seizures in these clinical settings occurred when inflammation was already present, an aspect not reproduced in animal studies pertaining to the effect of seizures on the developing brain. There is a reciprocal relationship between seizures and inflammatory cytokines (Vezzani and Granata, 2005). On the one hand, SE induced by kainic acid (KA) enhanced the expression of interleukin-1β (IL-1β) (Minami et al., 1990; Minami et al., 1991; Eriksson et al., 2000), interleukin-6, and tumor necrosis factor-α (TNF-α) (Vezzani et al., 1999; De Simoni et al., 2000). On the other hand, IL-1β prolonged KA-induced seizures (Vezzani et al., 1999). IL-1β