Gass Peter, Riva Marco A
Central Institute of Mental Health Mannheim, University of Heidelberg, Germany.
Bioessays. 2007 Oct;29(10):957-61. doi: 10.1002/bies.20658.
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.
转录因子CREB与抑郁症的发病机制及治疗相关的信号通路有关。与神经发生类似，慢性抗抑郁治疗可使海马体中的CREB上调并被激活。令人惊讶的是，最近一项使用CREB基因缺陷小鼠的研究也表明，神经发生的上调与抗抑郁行为表型相关。有趣的是，CREB基因缺陷小鼠对抗抑郁药表现出快速行为反应，而野生型小鼠则没有。本综述试图将这些新发现与关于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实验和未来的研究方向，这些研究可能会澄清一些悬而未决的问题。
