RETRACTED: Maternal adversity, glucocorticoids and programming of neuroendocrine function and behaviour (Retracted Article)

被引:157
作者
Owen, D
Andrews, MH
Matthews, SG
机构
[1] Univ Toronto, Fac Med, Dept Physiol, Toronto, ON M5S 1A8, Canada
[2] Univ Toronto, Fac Med, Dept Obstet & Gynecol, Toronto, ON M5S 1A8, Canada
[3] Univ Toronto, Fac Med, Dept Med, Toronto, ON M5S 1A8, Canada
关键词
prenatal stress; glucocorticoids; hypothalamo-pituitary-adrenal (HPA) axis; programming; hippocampus; perinatal; behaviour;
D O I
10.1016/j.neubiorev.2004.10.004
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
The fetus may be exposed to increased endogenous glucocorticoid or synthetic glucocorticoid in late gestation. Approximately 7% of pregnant women in Europe and North Arnerica are treated with synthetic glucocorticoid to promote lung maturation in fetuses at risk of preterm delivery. Very little is known about the mechanisms by which synthetic glucocorticoid or prenatal stress influence neurodevelopment in the human, or whether specific time windows of increased sensitivity exist. Glucocorticoids are essential for many aspects of normal brain development, but exposure of the fetal brain to excess glucocorticoid can have life-long effects on neuroendocrine function and behaviour. Both endogenous glucocorticoid and synthetic glucocorticoid exposure have a number of rapid effects in the fetal brain, including modification of neurotransmitter systems and transcriptional machinery. Such fetal exposure permanently alters hypothalamo-pituitary-adrenal (HPA) function in prepubertal, postpubertal and aging offspring, in a sex-dependent manner. Prenatal glucocorticoid manipulation also leads to modification of behaviour, brain and organ morphology, as well as altered regulation of other endocrine systems. Permanent changes in endocrine function will impact on health, since elevated cumulative exposure to endogenous glucocorticoid is linked to the premature onset of pathologies associated with aging. (c) 2004 Elsevier Ltd. All rights reserved.
引用
收藏
页码:209 / 226
页数:18
相关论文
共 206 条
[1]   Multiple courses of antenatal corticosteroids: A systematic review and meta-analysis [J].
Aghajafari, F ;
Murphy, K ;
Willan, A ;
Ohlsson, A ;
Amankwab, K ;
Matthews, S ;
Hannah, M .
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 2001, 185 (05) :1073-1080
[2]   Prenatal exposure to high levels of glucocorticoids increases the susceptibility of cerebellar granule cells to oxidative stress-induced cell death [J].
Ahlbom, E ;
Gogvadze, V ;
Chen, M ;
Celsi, G ;
Ceccatelli, S .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (26) :14726-14730
[3]   In vivo characterization of 11β-hydroxysteroid dehydrogenase in rat hippocampus using glucocorticoid neuroendangerment as an endpoint [J].
Ajilore, OA ;
Sapolsky, RM .
NEUROENDOCRINOLOGY, 1999, 69 (02) :138-144
[4]   The effects of prenatal stress on learning in rats in a morris maze [J].
Aleksandrov A.A. ;
Polyakova O.N. ;
Batuev A.S. .
Neuroscience and Behavioral Physiology, 2001, 31 (1) :71-74
[5]  
Alonso SJ, 2000, J PHYSIOL BIOCHEM, V56, P77, DOI 10.1007/BF03179902
[6]   Regulation of glucocorticoid receptor mRNA and heat shock protein 70 mRNA in the developing sheep brain [J].
Andrews, MH ;
Matthews, SG .
BRAIN RESEARCH, 2000, 878 (1-2) :174-182
[7]   Developmental regulation of the 5-HT7 serotonin receptor and transcription factor NGFI-A in the fetal guinea-pig limbic system: influence of GCs [J].
Andrews, MH ;
Kostaki, A ;
Setiawan, E ;
McCabe, L ;
Owen, D ;
Banjanin, S ;
Matthews, SG .
JOURNAL OF PHYSIOLOGY-LONDON, 2004, 555 (03) :659-670
[8]  
ANDREWS MH, 2003, FETAL MATERN MED REV, V14, P329, DOI DOI 10.1017/S0965539503001141
[9]   Differential regulation of glucocorticoid receptor messenger RNA (GR-mRNA) by maternal deprivation in immature rat hypothalamus and limbic regions [J].
Avishai-Eliner, S ;
Hatalski, CG ;
Tabachnik, E ;
Eghbal-Ahmadi, M ;
Baram, TZ .
DEVELOPMENTAL BRAIN RESEARCH, 1999, 114 (02) :265-268
[10]   EFFECTS OF MATERNAL AND SIBLING DEPRIVATION ON BASAL AND STRESS-INDUCED HYPOTHALAMIC-PITUITARY-ADRENAL COMPONENTS IN THE INFANT RAT [J].
AVISHAIELINER, S ;
YI, SJ ;
NEWTH, CJL ;
BARAM, TZ .
NEUROSCIENCE LETTERS, 1995, 192 (01) :49-52