NF-κB in the Nervous System

Abstract

The transcription factor NF-κB has diverse functions in the nervous system, depending on the cellular context. NF-κB is constitutively activated in glutamatergic neurons. Knockout of p65 or inhibition of neuronal NF-κB by super-repressor IκB resulted in the loss of neuroprotection and defects in learning and memory. Similarly, p50−/− mice have a lower learning ability and are sensitive to neurotoxins. Activated NF-κB can be transported retrogradely from activated synapses to the nucleus to translate short-term processes to long-term changes such as axon growth, which is important for long-term memory. In glia, NF-κB is inducible and regulates inflammatory processes that exacerbate diseases such as autoimmune encephalomyelitis, ischemia, and Alzheimer's disease. In summary, inhibition of NF-κB in glia might ameliorate disease, whereas activation in neurons might enhance memory. This review focuses on results produced by the analysis of genetic models.