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