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δ-连环蛋白是体内成熟皮质中维持神经结构和功能所必需的。

Delta-catenin is required for the maintenance of neural structure and function in mature cortex in vivo.

作者信息

Matter Cheryl, Pribadi Mochtar, Liu Xin, Trachtenberg Joshua T

机构信息

Department of Molecular and Medical Pharmacology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.

出版信息

Neuron. 2009 Nov 12;64(3):320-7. doi: 10.1016/j.neuron.2009.09.026.

Abstract

Delta-catenin is a brain-specific member of the adherens junction complex that localizes to the postsynaptic and dendritic compartments. This protein is likely critical for normal cognitive function; its hemizygous loss is linked to the severe mental retardation syndrome Cri-du-Chat and it directly interacts with presenilin-1 (PS1), the protein most frequently mutated in familial Alzheimer's disease. Here we examine dendritic structure and cortical function in vivo in mice lacking delta-catenin. We find that in cerebral cortex of 5-week-old mice, dendritic complexity, spine density, and cortical responsiveness are similar between mutant and littermate controls; thereafter, mutant mice experience progressive dendritic retraction, a reduction in spine density and stability, and concomitant reductions in cortical responsiveness. Our results indicate that delta-catenin regulates the maintenance of dendrites and dendritic spines in mature cortex but does not appear to be necessary for the initial establishment of these structures during development.

摘要

δ-连环蛋白是黏附连接复合体的一种脑特异性成员,定位于突触后和树突区室。这种蛋白质可能对正常认知功能至关重要;其半合子缺失与严重智力发育迟缓综合征猫叫综合征有关,并且它直接与早老素-1(PS1)相互作用,PS1是在家族性阿尔茨海默病中最常发生突变的蛋白质。在这里,我们研究了缺乏δ-连环蛋白的小鼠体内的树突结构和皮质功能。我们发现,在5周龄小鼠的大脑皮质中,突变体和同窝对照小鼠之间的树突复杂性、棘密度和皮质反应性相似;此后,突变小鼠经历渐进性树突回缩、棘密度和稳定性降低,以及皮质反应性随之降低。我们的结果表明,δ-连环蛋白调节成熟皮质中树突和树突棘的维持,但在发育过程中这些结构的初始建立似乎并非必需。

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