Bi-directional interaction of NF-κB in nervous system damage, learning and memory

The mechanism of action of nuclear factor-kappa B (NF-κB)'s has been widely studied in nervous system damage and disease since 2000. NF-κB is widely present in eukaryotic cells, and inactive NF-κB is present in the cytoplasm. Activated NF-κB transfers into the nucleus and induces expression of several target genes. Through the action of different downstream effectors, NF-κB plays a bi-directional interactive role in central nervous system damage, as well as learning and memory. While NF-κB can induce pro-inflammation factor release and exacerbate brain injury, it can also exert protective effects on neurons in central nervous system diseases and injuries by upregulating endothelial nitric oxide synthase (eNOS), Mn-superoxide dismutase (Mn-SOD), B-cell lymphoma/leukaemia-2 (Bcl-2), and inhibitors of apoptosis protein (IAPs). Moreover, NF-κB is required for spatial learning and memory and passive avoidance training. However, a decrease in NF-κB activity in the hippocampal dentate gyrus is necessary for active avoidance training. This paper reviews NF-κB's bi-directional interactive role in these processes.