title: NF-kappaB in the nervous system.
abstract: 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.
authors.affiliation: Molecular Neurobiology, University of Bielefeld, Universitätsstr. 25, D-33501 Bielefeld. barbara.kaltschmidt@uni-bielefeld.de
authors.forename: Barbara
authors.initials: B
authors.lastname: Kaltschmidt
authors.forename: Christian
authors.initials: C
authors.lastname: Kaltschmidt
mesh_terms: D000818:Animals; D006801:Humans; D007249:Inflammation; D008568:Memory; D051379:Mice; D008822:Mice, Transgenic; D008954:Models, Biological; D008957:Models, Genetic; D016328:NF-kappa B / Q000378:metabolism*; D052002:NF-kappa B p50 Subunit / Q000235:genetics; D009420:Nervous System; D009457:Neuroglia / Q000166:cytology; D009474:Neurons / Q000166:cytology; D010146:Pain; D013234:Stem Cells / Q000166:cytology
chemical_list: D016328:NF-kappa B; D052002:NF-kappa B p50 Subunit