SEIZURE-INDUCED NEURONAL INJURY - VULNERABILITY TO FEBRILE SEIZURES IN AN IMMATURE RAT MODEL

Febrile seizures are the most common seizure type in young children. W hether they induce death of hippocampal and amygdala neurons and conse quent limbic (temporal lobe) epilepsy has remained controversial, with conflicting data from prospective and retrospective studies. Using an appropriate-age rat model of febrile seizures, we investigated the ac ute and chronic effects of hyperthermic seizures on neuronal integrity and survival in the hippocampus and amygdala via molecular and neuroa natomical methods. Hyperthermic seizures-but not hyperthermia alone-re sulted in numerous argyrophilic neurons in discrete regions of the lim bic system; within 24 hr of seizures, a significant proportion of neur ons in the central nucleus of the amygdala and in the hippocampal CA3 and CA1 pyramidal cell layer were affected. These physicochemical alte rations of hippocampal and amygdala neurons persisted for at least 2 w eeks but were not accompanied by significant DNA fragmentation, as det ermined by in situ end labeling. By 4 weeks after the seizures, no sig nificant neuronal dropout in these regions was evident. In conclusion, in the immature rat model, hyperthermic seizures lead to profound, ye t primarily transient alterations in neuronal structure.