CREB, neurogenesis and depression
CREB, neurogenesis and depression
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DOI：
10.1002/bies.20658
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发表时间：
2007-10-01
期刊：
影响因子：
4
通讯作者：
Riva, Marco A.
中科院分区：
文献类型：
--
作者：
Gass, Peter;Riva, Marco A.
转录因子CREB参与了与抑郁症发病机制和治疗相关的信号通路。CREB在海马中被慢性抗抑郁治疗上调和激活，类似于神经发生。令人惊讶的是，最近一项使用CREB缺陷小鼠的研究也证明了与抗抑郁行为表型相关的神经发生上调。((1))有趣的是，CREB缺陷小鼠对抗抑郁药表现出快速的行为反应，而野生型小鼠则没有。这篇小综述试图将这些新发现与CREB，神经发生和抑郁症的既定概念相协调。它还概述了一些关键的实验和未来的研究路线，可以澄清一些悬而未决的问题。
The transcription factor CREB has been implicated in signalling pathways relevant for pathogenesis and therapy of depression. CREB is upregulated and activated in the hippocampus by chronic antidepressant treatment, similarly as neurogenesis. Surprisingly, a recent study using CREB-deficient mice also demonstrates an upregulation of neurogenesis correlating with an antidepressant behavioral phenotype.((1)) Interestingly, CREB-deficient mice show a rapid behavioral response to antidepressants, while wild-type mice do not. This minireview tries to reconcile these new findings with established concepts on CREB, neurogenesis and depression. It also outlines some crucial experiments and lines of future research that could clarify some of the pending questions.