Lifelong corticosterone level determines age-related decline in neurogenesis and memory

被引：143

作者：

Montaron, MF ^{[1
]}

Drapeau, E ^{[1
]}

Dupret, D ^{[1
]}

Kitchener, P ^{[1
]}

Aurousseau, C ^{[1
]}

Le Moal, M ^{[1
]}

Piazza, PV ^{[1
]}

Abrous, DN ^{[1
]}

机构：

[1] Univ Bordeaux 2, INSERM, Unite 588, Lab Physiopathol Comportement, F-33077 Bordeaux, France

来源：

NEUROBIOLOGY OF AGING | 2006年 / 27卷 / 04期

关键词：

neurogenesis; ageing; hippocampus; corticosterone; spatial learning;

D O I：

10.1016/j.neurobiolaging.2005.02.014

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

03 ; 0303 ; 100203 ;

摘要：

Ageing is accompanied by an alteration of spatial memory, a decline in hippocampal neurogenesis and a dysregulation of the hypothalamic-pituitary axis (HPA) leading to elevated levels of circulating corticosterone. However, the role of the HPA axis in age-related decline in cognitive functions and in neurogenesis decline remains unclear. We found that suppression of glucocorticoids secretion from midlife to the rest of the animals' life increases neurogenesis in old animals and prevents the emergence of age-related memory disorders. Reciprocally, aged rats with a chronic upregulation of the HPA axis exhibit not only spatial memory impairments but also very low levels of hippocampal cell proliferation and survival. Altogether, these results indicate that the extent of lifetime exposure to glucocorticoids determines the extent of age-related decline in hippocampal neurogenesis and consequently age-related cognitive dysfunctions. (C) 2005 Elsevier Inc. All rights reserved.

引用

页码：645 / 654

页数：10

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