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Journal of Neuroscience, Vol 14, 3998-4006, Copyright © 1994 by Society for Neuroscience
Prolonged expression of AP-1 transcription factors in the rat hippocampus after systemic kainate treatment
KR Pennypacker, L Thai, JS Hong and MK McMillian
Neuropharmacology Section, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, North Carolina 27709.
Systemic administration of kainate, a glutamate receptor agonist, caused
neuronal death in the CA1 and CA3 fields of the rat hippocampus. In the
areas of cell loss, reactive astrocytes increased their expression of an
astrocyte-specific protein, glial fibrillary acidic protein (GFAP). AP-1
DNA binding activity and the expression of a 35 kDa fos-related antigen
(fra) remained elevated in the rat hippocampus for at least 2 weeks after a
single systemic injection of kainate, which correlated with changes in gene
expression during reactive gliosis. Immunoreactivity for fras was detected
in the nuclei of neurons in the dentate gyrus, but relatively few cells in
CA1 and CA3 were immunoreactive 1 week after kainate treatment. However,
elevated AP-1 DNA binding activity was observed in the CA1 and CA3 regions
as well as in the dentate gyrus, suggesting that proteins other than the
fras were involved in the astrocytic AP-1 complex. The AP-1 DNA binding
activity in hippocampus recognized an AP-1 sequence from the promoter
region of the GFAP gene, suggesting that GFAP is a potential target gene.
Thus, a single systemic injection of kainate causes long-term activation of
AP-1 DNA binding activity in the rat hippocampus and may be important for
long-term changes in gene expression in hippocampal cells.
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