Dextromethorphan blocks opioid peptide gene expression in the rat hippocampus induced by kainic acid

H. C. Kim, H. W. Suh, D. Bronstein, G. Bing, B. Wilson, J. S. Hong

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


We have previously shown that dextromethorphan (DM) antagonizes kainic acid (KA)-induced neurotoxicity. Accumulating evidence indicates that the induction of seizure activity causes profound alterations in the levels of hippocampal opioid peptide mRNA. The present study was performed to further explore the effect of DM on KA-induced seizures as measured by hippocampal opioid peptide mRNA levels. Both Northern blot and in situ hybridization methods were used to examine the proenkephalin (PENK) and prodynorphin (PDYN) mRNA levels in the rat hippocampus. The robust seizure activity induced by KA correlated with a significant increase in hippocampal opioid peptide mRNA levels. Pretreatment of rats with DM decreased hippocampal PENK and PDYN mRNA levels and seizure activity induced by KA. Hippocampal PDYN mRNA levels fell quickly but PENK mRNA levels fell rather slowly, indicating that the PENK and PDYN mRNAs are differentially regulated. Our results demonstrate that DM modulates opioid peptide gene expression induced by KA, and that DM protects against KA-induced seizures.

Original languageEnglish
Pages (from-to)105-112
Number of pages8
Issue number2
StatePublished - 1997

Bibliographical note

Funding Information:
This research was partially supported by the Korea Science & Engineering Foundation (KOSEF 95-0403-19-01-3). We would like to thank Dr Maderdrut for his critical reading of this manuscript.

ASJC Scopus subject areas

  • Endocrinology
  • Neurology
  • Endocrine and Autonomic Systems
  • Cellular and Molecular Neuroscience


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