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Induction of NF‐kB‐like transcription factors in brain areas susceptible to kainate toxicity

Induction of NF‐kB‐like transcription factors in brain areas susceptible to kainate toxicity Administration of kainate (KA), a glutamate receptor agonist, to rats causes neuronal damage in the CA1/CA3 fields of the hippocampus and in the pyriform/entorhinal cortex. Reactive gliosis also occurs and activated astrocytes upregulate their expression of a large number of molecules. Since NF‐kB transcription factors are involved in cellular responses to diverse pathogenic stimuli and have been shown to be induced in astrocytes in vitro in response to cytokines and growth factors, we investigated their possible involvement in the changes in gene expression subsequent to KA‐induced lesions. Immunoreactivity to the p65 subunit of NF‐kB was markedly increased in non‐neuronal cells 2 days after KA administration (8 mg/kg i.p.) in the areas of selective neuronal degeneration. This increase was not observed 3 h or 1 day after injection, but was still present 7–10 days after KA injection. By gel mobility‐shift assay, a protein complex binding to the kB consensus sequence was found to be induced by 2 days after KA, which correlated with immunohistochemical findings. This NF‐kB‐protein complex seemed to be localized in reactive astrocytes, as indicated by the morphological similarity of NF‐kB‐positive cells and reactive astrocytes stained with glial fibrillary acidic protein (GFAP) antibody, and the parallelism between the time course of NF‐kB induction and appearance of gliosis after KA treatment. Double immunocytochemistry experiments demonstrated the colocalization of NF‐kB positive cells and reactive astrocytes. Our results suggest that activated NF‐kB in astrocytes participates in delayed and long‐term responses of glia to injury. © 1996 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Glia Wiley

Induction of NF‐kB‐like transcription factors in brain areas susceptible to kainate toxicity

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References (41)

Publisher
Wiley
Copyright
Copyright © 1996 Wiley‐Liss, Inc.
ISSN
0894-1491
eISSN
1098-1136
DOI
10.1002/(SICI)1098-1136(199604)16:4<306::AID-GLIA3>3.0.CO;2-Y
Publisher site
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Abstract

Administration of kainate (KA), a glutamate receptor agonist, to rats causes neuronal damage in the CA1/CA3 fields of the hippocampus and in the pyriform/entorhinal cortex. Reactive gliosis also occurs and activated astrocytes upregulate their expression of a large number of molecules. Since NF‐kB transcription factors are involved in cellular responses to diverse pathogenic stimuli and have been shown to be induced in astrocytes in vitro in response to cytokines and growth factors, we investigated their possible involvement in the changes in gene expression subsequent to KA‐induced lesions. Immunoreactivity to the p65 subunit of NF‐kB was markedly increased in non‐neuronal cells 2 days after KA administration (8 mg/kg i.p.) in the areas of selective neuronal degeneration. This increase was not observed 3 h or 1 day after injection, but was still present 7–10 days after KA injection. By gel mobility‐shift assay, a protein complex binding to the kB consensus sequence was found to be induced by 2 days after KA, which correlated with immunohistochemical findings. This NF‐kB‐protein complex seemed to be localized in reactive astrocytes, as indicated by the morphological similarity of NF‐kB‐positive cells and reactive astrocytes stained with glial fibrillary acidic protein (GFAP) antibody, and the parallelism between the time course of NF‐kB induction and appearance of gliosis after KA treatment. Double immunocytochemistry experiments demonstrated the colocalization of NF‐kB positive cells and reactive astrocytes. Our results suggest that activated NF‐kB in astrocytes participates in delayed and long‐term responses of glia to injury. © 1996 Wiley‐Liss, Inc.

Journal

Glia – Wiley

Published: Apr 1, 1996

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