Stress In Utero: Prenatal Programming of Brain Plasticity and Cognition

被引:166
作者
Bock, Joerg [1 ]
Wainstock, Tamar [2 ]
Braun, Katharina [1 ]
Segal, Menahem [3 ]
机构
[1] Univ Magdeburg, Ctr Behav Brain Sci, D-39106 Magdeburg, Germany
[2] Emory Univ, Rollins Sch Publ Hlth, Atlanta, GA 30322 USA
[3] Weizmann Inst Sci, Dept Neurobiol, IL-76100 Rehovot, Israel
关键词
Cognitive impairments; Dendritic spines; Epigenetics; Prenatal stress; Synaptic plasticity; ANTENATAL MATERNAL ANXIETY; DNA METHYLATION; NORADRENERGIC MODULATION; PREFRONTAL CORTEX; RESTRAINT STRESS; SPINE DENSITY; BIRTH-WEIGHT; PSYCHOLOGICAL DISTRESS; EPIGENETIC MECHANISMS; CORTICOSTERONE LEVELS;
D O I
10.1016/j.biopsych.2015.02.036
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Animal studies confirm earlier anecdotal observations in humans to indicate that early life experience has a profound impact on adult behavior, years after the original experience has vanished. These studies also highlight the role of early life adversaries in the shaping of a disordered brain. Evidence is accumulating to indicate that the epigenome, through which the environment regulates gene expression, is responsible for long-lasting effects of stress during pregnancy on brain and behavior. A possible differential effect of the environment on the epigenome may underlie the observation that only a small fraction of a population with similar genetic background deteriorates into mental disorders. Considerable progress has been made in the untangling of the epigenetic mechanisms that regulate emotional brain development. The present review focuses on the lasting effects of prenatal stress on brain plasticity and cognitive functions in human and rodent models. Although human studies stress the significance of early life experience in functional maturation, they lack the rigor inherent in controlled animal experiments. Furthermore, the analysis of molecular and cellular mechanisms affected by prenatal stress is possible only in experimental animals. The present review attempts to link human and animal studies while proposing molecular mechanisms that interfere with functional brain development.
引用
收藏
页码:315 / 326
页数:12
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