Abstracts

Rationale: Prolonged febrile seizures (PFZ) have been associated with the mesial temporal lobe epilepsy syndrome. Although a number of factors contributing to febrile seizures have been identified, still much debate exists on the consequences. In the past few years, altered neurogenesis, inflammation, as well as cell death have been proposed as a mechanism by which seizures modulate the brain plasticity. In this study, we tested whether hyperthermia-induced seizures would result in the epileptogenic changes described in animal model with temporal lobe epilepsy. In addition, we examined if erythropoietin (EPO) could prevent these changes and attenuate the epilepsy formation. Methods: Febrile seizures were induced by an adjustable stream of heated air for 30 minutes with body temperature monitoring. The rats were assigned to EPO (5000IU/kg) or saline-treated groups, and sacrificed at 1, 3, 7, 14, 60 days after hyperthermia for analyzing the inflammation or plasticity-related changes.Results: EPO significantly reduced the brain edema and TNF-α expression at the 1, 3 days following PFZ. Mild increase of microglia was observed in the two groups, but more increase in saline-group than EPO-group in the 14- and 60-day brains. EPO reduced the upregulation of cystatin C following PFZ. Subsequently, EPO attenuated the frequencies of spontaneous recurrent seizures at 3, and 5 months after PFZ.Conclusions: In conclusion, inflammation, BBB breakdown, chemokines, or plasticity-related molecules occur in the rat brain with PFZ. EPO might prevent the epileptogenesis via modulation of these factors.