Chourbaji Sabine, Gass Peter
Central Institute of Mental Health (ZI), J5, Mannheim, D-68159, Germany.
Brain Res Rev. 2008 Mar;57(2):554-60. doi: 10.1016/j.brainresrev.2007.04.008. Epub 2007 May 3.
In the era of mutant mice generated as molecular in vivo models for complex pathogenetic and therapeutic aspects of particular human diseases, glucocorticoid receptor transgenic mice represent an interesting and promising tool. Animals carrying mutations of this receptor show alterations in the hypothalamic-pituitary-adrenal (HPA)-system, which are comparable to those observed in depressed patients. Furthermore, similarities that may model the human disease have been described on the behavioral and pharmacological level, which increase the impact of such mutants. In this review we summarize different approaches used to alter or eliminate glucocorticoid receptor expression and function, and discuss their relevance as models for depression.
在通过基因改造培育出突变小鼠作为特定人类疾病复杂发病机制和治疗方法的分子体内模型的时代,糖皮质激素受体转基因小鼠是一种有趣且有前景的工具。携带该受体突变的动物下丘脑 - 垂体 - 肾上腺(HPA)系统会出现改变,这与在抑郁症患者中观察到的情况类似。此外,在行为和药理学层面也描述了可能模拟人类疾病的相似之处,这增加了此类突变体的影响力。在本综述中,我们总结了用于改变或消除糖皮质激素受体表达及功能的不同方法,并讨论它们作为抑郁症模型的相关性。