Developmental regulation of glutamate and gabaa receptor gene expression in rat hippocampus following kainate-induced status epilepticus

Linda K. Friedman, Ellen F. Sperber, Solomon L. Moshe, Michael V. Bennett, R. Suzanne Zakin

Research output: Contribution to journalArticlepeer-review

62 Scopus citations


In adult rats, kainic acid-induced status epilepticus markedly reduces GluR2 (the α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid, AMPA subunit that limits Ca2+ permeability), receptor mRNA in the vulnerable CA3 and may contribute to delayed neurodegeneration. In rat pups resistant to kainate seizure-induced hippocampal neurodegeneration by silver impregnation, glutamate or GABAA α1-receptor mRNAs were unaltered in CA3 neurons 24 h after status epilepticus. In the dentate gyrus, GluR1 and GluR2 mRNAs were transiently increased in P14 but not P5 pups. Immunocytochemistry revealed no apparent differences in the distribution patterns of GluR1, GluR2, or GluR2/3 receptor proteins in the CA3 or dentate gyrus of P14 pups. Status epilepticus-induced alterations in receptor GluR2 and GABAA α1 mRNAs and AMPA protein expression vary with developmental age. Sustained expression at young ages may contribute to the resistance of developing hippocampal neurons to seizure-induced damage.

Original languageEnglish (US)
Pages (from-to)529-542
Number of pages14
JournalDevelopmental Neuroscience
Issue number6
StatePublished - Jan 1997


  • AMPA receptors
  • Developing rat brain
  • Epilepsy
  • GABA receptors
  • Gene expression
  • Hybridization in situ
  • Kainic acid
  • NMDA receptors
  • Seizures
  • Silver impregnation

ASJC Scopus subject areas

  • Neurology
  • Developmental Neuroscience


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