[background] Status epilepticus (SE) with fever is common disease in children, but it contains various origins, such as febrile seizure, acute encephalopathy, and acute meningitis. Exact diagnosis in acute phase and clarifying the clinical state are important, because SE occasionally induces heavy sequel. We check the quantitative analysis of inhibitory neurons to investigate the relationship between SE and the sequel by the model mouse of SE. [method] Jcl:ICR and C57BL/6J mice are used for experiment at P15. Lipopolysaccharide (LPS) 1mg/kg or poly(I:C) 10mg/kg have been used to activate the immunity, an hour after that, 1mg/kg scopolamine and 200mg/kg pilocarpine have been used to induce the seizure. After 3 days, mRNA have extracted from the neocortex and the hippocampus. Quantitative analysis by real time PCR determines the transcripts of inflammatory cytokines (TNFα, IL1β, IL6), proteins in relation to inhibitory neurons (Parvalbmin: PV, Somatostatin: SOM, Calretinin: CR), and so on. The other mice are fixed with 4% paraformaldehyde (PFA). The Fixed brains have sliced, immunostained and evaluate by confocal microscopy. Moreover, at P30 we check the behavior evaluation (open field test, fear conditioning test), and the transcripts of neocortex and hippocampus are analyzed and brain slices are immunostained. We examine the correlation between the severity of SE and the presence and severity of autism and disturbance of cognition. [result] Seizure has not been induced by only LPS or poly(I:C). In the immunostaining, PV immunoreactivity has been reduced by pilocarpine-induced seizure. This trend was forced by inflammation made by LPS and poly(I:C). Moreover, the quantitative RT-PCR shows that pilocarpine-induced seizure inhibits the expression of PV and GABA-A receptor α1 subunit. We are going to do the behavior evaluation, and we check the correlation between the reduction of inhibitory neurons by pilocarpine and severity of disturbance of cognition. [conclusion] The pilocarpine-induced seizure reduces the PV positive inhibitory neurons in the hippocampus and neocortex, and it may relate to the cause of the sequel of SE.