Abstract
Nuclear factor-κB (NF-κB) is known to play a key role in immune and inflammatory responses. To understand the mechanisms of inflammatory activation that accompany neuronal damage, we determined the cell type in which NF-κB was activated. NF-κB protein was detected in the cytosolic fraction of untreated and vehicle-treated rat hippocampus. After kainic acid (KA) treatment, NF-κB protein was significantly increased in both the cytosolic and particulate fractions. NF-κB immunoreactivity was observed in both brain blood vessels and glial cells after 1 day. Although NF-κB immunoreactivity in brain blood vessels disappeared after 3 days, this activity was maintained in glial cells for up to 7 days. In addition, double immunostaining indicates that NF-κB was activated in glial cells, such as microglia and astrocytes, after 3 days. Thus, NF-κB activation seems to be delayed and to occur continuously in microglia and astrocytes, suggesting that an inflammatory activation in glial cells participates in KA-induced neurodegeneration.
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Received: 2 September 1997 / Accepted: 28 July 1998
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Matsuoka, Y., Kitamura, Y., Okazaki, M. et al. Kainic acid-induced activation of nuclear factor-κB in rat hippocampus. Exp Brain Res 124, 215–222 (1999). https://doi.org/10.1007/s002210050616
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DOI: https://doi.org/10.1007/s002210050616