NF-κB in the Nervous System
NF-κB in the Nervous System
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DOI：
10.1101/cshperspect.a001271
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发表时间：
2009-09-01
影响因子：
7.2
通讯作者：
Kaltschmidt, Christian
中科院分区：
文献类型：
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作者：
Kaltschmidt, Barbara;Kaltschmidt, Christian
转录因子 NF-kappa B 在神经系统中具有多种功能，具体取决于细胞环境。 NF-κ B 在谷氨酸能神经元中被组成型激活。敲除 p65 或通过超级阻遏物 I kappa B 抑制神经元 NF-kappa B 会导致神经保护丧失以及学习和记忆缺陷。同样，p50(-/-)小鼠的学习能力较低，对神经毒素敏感。激活的 NF-κ B 可以从激活的突触逆行转运到细胞核，将短期过程转化为长期变化，例如轴突生长，这对长期记忆很重要。在神经胶质细胞中，NF-κ B 可诱导并调节炎症过程，从而加剧自身免疫性脑脊髓炎、缺血和阿尔茨海默病等疾病。总之，抑制神经胶质细胞中的 NF-κ B 可能会改善疾病，而激活神经元可能会增强记忆。本综述重点关注遗传模型分析产生的结果。
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.