Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9429857 | Neuroscience Letters | 2005 | 5 Pages |
Abstract
NF-κB is a nuclear transcription factor involved in the control of fundamental cellular functions including cell survival. Among the many target genes of this factor, both pro- and anti-apoptotic genes have been described. To evaluate the contribution of NF-κB activation to excitotoxic insult, we analysed the effect of IkappaBalpha (IκBα) phosphorylation blockade on glutamate-induced toxicity in adult mouse hippocampal slices. By using immunocytochemical and EMSA techniques, we found that (i) acute exposure of hippocampal slices to NMDA induced nuclear translocation of NF-κB, (ii) NMDA-mediated activation of NF-κB was prevented by BAY 11-7082, an inhibitor of IκBα phosphorylation and degradation, and (iii) BAY 11-7082-mediated inhibition of NF-κB activation was associated with neuroprotection.
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Authors
F. Goffi, F. Boroni, M. Benarese, I. Sarnico, A. Benetti, P.F. Spano, M. Pizzi,