Seizure-induced neuronal injury: Vulnerability to febrile seizures in an immature rat model

Zsolt Toth, Xiao Xin Yan, Suzie Haftoglou, Charles E. Ribak, Tallie Z. Baram

Research output: Contribution to journalArticle

214 Citations (Scopus)

Abstract

Febrile seizures are the most common seizure type in young children. Whether they induce death of hippocampal and amygdala neurons and consequent 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 acute and chronic effects of hyperthermic seizures on neuronal integrity and survival in the hippocampus and amygdala via molecular and neuroanatomical methods. Hyperthermic seizures-but not hyperthermia alone-resulted in numerous argyrophilic neurons in discrete regions of the limbic system; within 24 hr of seizures, a significant proportion of neurons in the central nucleus of the amygdala and in the hippocampal CA3 and CA1 pyramidal cell layer were affected. These physicochemical alterations of hippocampal and amygdala neurons persisted for at least 2 weeks but were not accompanied by significant DNA fragmentation, as determined by in situ end labeling. By 4 weeks after the seizures, no significant neuronal dropout in these regions was evident. In conclusion, in the immature rat model, hyperthermic seizures lead to profound, yet primarily transient alterations in neuronal structure.

Original languageEnglish
Pages (from-to)4285-4294
Number of pages10
JournalJournal of Neuroscience
Volume18
Issue number11
DOIs
Publication statusPublished - Jun 1 1998

Keywords

  • Animal model
  • Apoptosis
  • Epilepsy
  • Excitotoxicity
  • Febrile seizures
  • In situ end labeling
  • Neuronal death
  • Seizures

ASJC Scopus subject areas

  • Neuroscience(all)

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