Regulation of Adult Neurogenesis and Plasticity by (Early) Stress, Glucocorticoids, and Inflammation

被引:109
作者
Lucassen, Paul J. [1 ]
Oomen, Charlotte A. [1 ]
Naninck, Eva F. G. [1 ]
Fitzsimons, Carlos P. [1 ]
van Dam, Anne-Marie [2 ]
Czeh, Boldizsar [3 ,4 ]
Korosi, Aniko [1 ]
机构
[1] Univ Amsterdam, Ctr Neurosci, Swammerdam Inst Life Sci, NL-1090 GE Amsterdam, Netherlands
[2] Vrije Univ Amsterdam Med Ctr, Dept Anat & Neurosci, NL-1007 MB Amsterdam, Netherlands
[3] Univ Pecs, Neurobiol Stress Res Grp, MTA PTE, H-7624 Pecs, Hungary
[4] Univ Pecs, Struct Neurobiol Res Grp, Szentagothai Janos Res Ctr, H-7624 Pecs, Hungary
关键词
EARLY-LIFE STRESS; CHRONIC PSYCHOSOCIAL STRESS; NEURAL PROGENITOR CELLS; RAT DENTATE GYRUS; ANTAGONIST MIFEPRISTONE NORMALIZES; EARLY MATERNAL-DEPRIVATION; MAJOR DEPRESSIVE DISORDER; HIPPOCAMPAL NEUROGENESIS; CORTICOSTEROID RECEPTORS; ANTIDEPRESSANT TREATMENT;
D O I
10.1101/cshperspect.a021303
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Exposure to stress is one of the best-known negative regulators of adult neurogenesis (AN). We discuss changes in neurogenesis in relation to exposure to stress, glucocorticoid hormones, and inflammation, with a particular focus on early development and on lasting effects of stress. Although the effects of acute and mild stress on AN are generally brief and can be quickly overcome, chronic exposure or more severe forms of stress can induce longer lasting reductions in neurogenesis that can, however, in part, be overcome by subsequent exposure to exercise, drugs targeting the stress system, and some antidepressants. Exposure to stress, particularly during the sensitive period of early life, may (re) program brain plasticity, in particular, in the hippocampus. This may increase the risk to develop cognitive or anxiety symptoms, common to brain diseases like dementia and depression in which plasticity changes occur, and a normalization of neurogenesis may be required for a successful treatment response and recovery.
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页数:16
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