Kaltschmidt Barbara, Widera Darius, Kaltschmidt Christian
Institut für Neurobiochemie Universität Witten/Herdecke, Stockumer Street 10, D-58448 Witten, Germany.
Biochim Biophys Acta. 2005 Sep 30;1745(3):287-99. doi: 10.1016/j.bbamcr.2005.05.009.
Nuclear factor kappa B (NF-kappaB) is an inducible transcription factor present in neurons and glia. Recent genetic models identified a role for NF-kappaB in neuroprotection against various neurotoxins. Furthermore, genetic evidence for a role in learning and memory is now emerging. This review highlights our current understanding of neuronal NF-kappaB in response to synaptic transmission and summarizes potential physiological functions of NF-kappaB in the nervous system. This article contains a listing of NF-kappaB activators and inhibitors in the nervous system, furthermore specific target genes are discussed. Synaptic NF-kappaB activated by glutamate and Ca2+ will be presented in the context of retrograde signaling. A controversial role of NF-kappaB in neurodegenerative diseases will be discussed. A model is proposed explaining this paradox as deregulated physiological NF-kappaB activity, where novel results are integrated, showing that p65 could be turned from an activator to a repressor of anti-apoptotic genes.
核因子κB（NF-κB）是一种存在于神经元和神经胶质细胞中的可诱导转录因子。最近的基因模型确定了NF-κB在抵抗各种神经毒素的神经保护作用。此外，现在也出现了其在学习和记忆中发挥作用的遗传学证据。本综述重点介绍了我们目前对神经元NF-κB对突触传递反应的理解，并总结了NF-κB在神经系统中的潜在生理功能。本文列出了神经系统中的NF-κB激活剂和抑制剂，此外还讨论了特定的靶基因。由谷氨酸和Ca2+激活的突触NF-κB将在逆行信号传导的背景下进行介绍。将讨论NF-κB在神经退行性疾病中的争议性作用。提出了一个模型来解释这种矛盾现象，即生理NF-κB活性失调，其中整合了新的结果，表明p65可以从抗凋亡基因的激活剂转变为抑制剂。
