Referenced in: none

Automatically associated channels: Slo1

Title: Calcium signal-initiated early activation of NF-kappaB in neurons is a neuroprotective event in response to kainic acid-induced excitotoxicity.

Authors: Shu-Yan Li, Wen-Ge Sun, Yu-Hong Jia, Guo-Sheng Wu, Guo-Shun An, Ju-Hua Ni, Hong-Ti Jia

Journal, date & volume: Biochemistry Mosc., 2010 Jan , 75, 101-9

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/20331430

Abstract
We demonstrate that activation of nuclear factor kappaB (NF-kappaB) in neurons is neuroprotective in response to kainic acid (KA)-induced excitotoxicity. Combination of Western blotting, immunocytochemistry, and electrophoresis mobility shift assay showed that KA exposure induced a fast but transient nuclear translocation of the NF-kappaB p65 subunit and increased DNA-binding activity of NF-kappaB in primary cultured cortical neurons. The transient NF-kappaB activity was associated with upregulation of antiapoptotic Bcl-xL and XIAP gene products revealed by real-time PCR. Knockdown of p65 decreased neuronal viability and antiapoptotic gene expression. In addition, we showed that KA-stimulated DNA-binding activity of NF-kappaB was associated with reactive oxygen species and calcium signals, using AMPA/KA receptor antagonist, calcium chelator, and antioxidant. These results suggest that the fast and transient activation of NF-kappaB initiated by calcium signals is one of the important proximal events in response to KA-induced excitotoxicity, which has neuroprotective effect against KA-induced apoptosis.