Kainic acid-induced activation of nuclear factor-kappaB in rat hippocampus.

Nuclear factor-kappaB (NF-kappaB) 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-kappaB was activated. NF-kappaB protein was detected in the cytosolic fraction of untreated and vehicle-treated rat hippocampus. After kainic acid (KA) treatment, NF-kappaB protein was significantly increased in both the cytosolic and particulate fractions. NF-kappaB immunoreactivity was observed in both brain blood vessels and glial cells after 1 day. Although NF-kappaB 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-kappaB was activated in glial cells, such as microglia and astrocytes, after 3 days. Thus, NF-kappaB 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.