期刊
COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY
卷 1, 期 3, 页码 -出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/cshperspect.a001271
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The transcription factor NF-kappa B has diverse functions in the nervous system, depending on the cellular context. NF-kappa B is constitutively activated in glutamatergic neurons. Knockout of p65 or inhibition of neuronal NF-kappa B by super-repressor I kappa B 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-kappa B 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-kappa B is inducible and regulates inflammatory processes that exacerbate diseases such as autoimmune encephalomyelitis, ischemia, and Alzheimer's disease. In summary, inhibition of NF-kappa B in glia might ameliorate disease, whereas activation in neurons might enhance memory. This review focuses on results produced by the analysis of genetic models.
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