NF-kappaB in the nervous system

Cold Spring Harb Perspect Biol. 2009 Sep;1(3):a001271. doi: 10.1101/cshperspect.a001271.


The transcription factor NF-kappaB has diverse functions in the nervous system, depending on the cellular context. NF-kappaB is constitutively activated in glutamatergic neurons. Knockout of p65 or inhibition of neuronal NF-kappaB by super-repressor IkappaB 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-kappaB 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-kappaB is inducible and regulates inflammatory processes that exacerbate diseases such as autoimmune encephalomyelitis, ischemia, and Alzheimer's disease. In summary, inhibition of NF-kappaB in glia might ameliorate disease, whereas activation in neurons might enhance memory. This review focuses on results produced by the analysis of genetic models.

Publication types

  • Review

MeSH terms

  • Animals
  • Humans
  • Inflammation
  • Memory
  • Mice
  • Mice, Transgenic
  • Models, Biological
  • Models, Genetic
  • NF-kappa B / metabolism*
  • NF-kappa B p50 Subunit / genetics
  • Nervous System*
  • Neuroglia / cytology
  • Neurons / cytology
  • Pain
  • Stem Cells / cytology


  • NF-kappa B
  • NF-kappa B p50 Subunit