Kainate‐Induced Changes in Opioid Peptide Genes and AP‐1 Protein Expression in the Rat Hippocampus

Keith R. Pennypacker(National Institute of Environmental Health Sciences), D. Walczak(Solvay (Belgium)), L. Thai(National Institutes of Health), Rickie D. Fannin(National Institutes of Health), Elizabeth A. Mason(National Institutes of Health), J Douglass(Vollum Institute), Jau‐Shyong Hong(National Institutes of Health)
Journal of Neurochemistry
January 1, 1993
Cited by 66

Abstract

In the rat hippocampus, jun, c-fos, and fos-related antigen immunoreactivity, AP-1 DNA binding, and opioid peptide gene expression were examined after kainate treatment to determine whether the induction and DNA binding of AP-1 transcription factors are correlated with the expression of the opioid peptide genes. One and one-half hours after kainate administration, fos-related antigen and jun immunoreactivity and AP-1 DNA binding were induced; maximal elevation was observed after 4.5 h. Transcription factor expression and DNA binding increased in a dose-dependent manner. Preprodynorphin and preproenkephalin mRNA induction was also dose dependent. The anticonvulsants, pentobarbital and diazepam, effectively blocked electroencephalographic seizure activity caused by kainate treatment, whereas valproic acid was approximately 50% effective. Opioid peptide gene expression, fos-related antigen and jun immunoreactivity, and AP-1 DNA binding all reflected similar reductions after anticonvulsant treatment. Therefore, expression and DNA binding activity of the AP-1 transcription factors are correlated with opioid peptide gene expression in the rat hippocampus.


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