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Kainate‐Induced Changes in Opioid Peptide Genes and AP‐1 Protein Expression in the Rat Hippocampus
Author(s) -
Pennypacker K. R.,
Walczak D.,
Thai L.,
Fannin R.,
Mason E.,
Douglass J.,
Hong J. S.
Publication year - 1993
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1993.tb05839.x
Subject(s) - kainate receptor , gene expression , microbiology and biotechnology , kainic acid , opioid peptide , chemistry , biology , opioid , medicine , endocrinology , gene , biochemistry , receptor , glutamate receptor , ampa receptor
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.