Differential Effect of Prenatal Stress on the Expression of Cortiocotrophin-Releasing Hormone and its Receptors in the Hypothalamus and Amygdala in Male and Female Rats

Zohar, Inbar; Weinstock, Marta

doi:10.1111/j.1365-2826.2011.02117.x

Cited by 97 publications

(90 citation statements)

References 56 publications

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“…Kirschbaum et al, 1995; 1992) and, as shown in animal studies, also moderates the effects of environmental stress and stress-system genes on the HPA axis and the limbic system (e.g. Bourke et al, 2013; Shors et al, 2001; Zohar and Weinstock, 2011). In addition, stress reactivity has a particularly strong effect on emotion processing during puberty (e.g.…”

Section: Introductionmentioning

confidence: 75%

HPA axis genetic variation, pubertal status, and sex interact to predict amygdala and hippocampus responses to negative emotional faces in school-age children

et al. 2015

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Accumulating evidence suggests a role for stress exposure, particularly during early life, and for variation in genes involved in stress response pathways in neural responsivity to emotional stimuli. Understanding how individual differences in these factors predict differences in emotional responsivity may be important for understanding both normative emotional development and for understanding the mechanisms underlying internalizing disorders, like anxiety and depression, that have often been related to increased amygdala and hippocampus responses to negatively valenced emotional stimuli. The present study examined whether stress exposure and genetic profile scores (10 single nucleotide polymorphisms within four hypothalamic-pituitary-adrenal axis genes: CRHR1, NR3C2, NR3C1, and FKBP5) predict individual differences in amygdala and hippocampus responses to fearful vs. neutral faces in school-age children (7–12 year olds; N=107). Experience of more stressful and traumatic life events predicted greater left amygdala responses to negative emotional stimuli. Genetic profile scores interacted with sex and pubertal status to predict amygdala and hippocampus responses. Specifically, genetic profile scores were a stronger predictor of amygdala and hippocampus responses among pubertal vs. prepubertal children where they positively predicted responses to fearful faces among pubertal girls and positively predicted responses to neutral faces among pubertal boys. The current results suggest that genetic and environmental stress-related factors may be important in normative individual differences in responsivity to negative emotional stimuli, a potential mechanism underlying internalizing disorders. Further, sex and pubertal development may be key moderators of the effects of stress-system genetic variation on amygdala and hippocampus responsivity, potentially relating to sex differences in stress-related psychopathology.

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Section: Introductionmentioning

confidence: 75%

HPA axis genetic variation, pubertal status, and sex interact to predict amygdala and hippocampus responses to negative emotional faces in school-age children

et al. 2015

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“…This differential CRH receptor mRNA expression in the amygdaloid complex in prenatally stressed males and females may underlie the difference in anxiety-like behaviour following social stress exposure in late gestation. Indeed, in other prenatal stress models where both sexes exhibit heightened anxiety, reduced Crhr2 expression is observed in the amygdala in both sexes (Zohar & Weinstock 2011). It is not known whether these changes in CRH receptor expression in the amygdala result from changes in DNA methylation in the promoter regions of the CRH receptor genes, as has been shown for Crhr1 mRNA expression in the PVN in anxious male offspring of mothers exposed to hypoxia throughout gestation (Wang et al 2013).…”

Section: Effects On Anxiety-like Behaviour In Prenatally Stressed Offmentioning

confidence: 94%

Effects of maternal exposure to social stress during pregnancy: consequences for mother and offspring

2013

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A suboptimal in utero environment, for example, as a result of maternal stress, can have detrimental effects on the pregnancy and long-term adverse 'programming' effects on the offspring. This article focuses on the effects of prenatal social stress on the mother, her pregnancy and the offspring, since these issues have ethological relevance in both animals and humans. The consequences of social stress exposure depend on when during pregnancy the stress occurs, and many of the effects on the offspring are sex specific. Social stress during early pregnancy tends to result in pregnancy loss, whereas stress exposure later in pregnancy, when the mother has already invested considerable resources in the foetuses, results in programmed offspring of low birth weight: a risk factor for various adulthood diseases. Neuroendocrine and behavioural responses to stress in the offspring are particularly sensitive to foetal programming by prenatal stress, indicated by enhanced hypothalamo-pituitary-adrenal (HPA) axis responses and increased anxiety behaviour, which result from permanent changes in the offspring's brain. The dysregulation of HPA axis function may also interfere with other systems, for example, the hypothalamic-pituitary-gonadal axis, as there is evidence for alterations in steroidogenesis, reproductive potential and impaired reproductive/social behaviours in prenatally stressed offspring. Prenatal social stress also programmes future maternal behaviour, highlighting the potential for negative phenotypes to be transmitted to future generations. The possible mechanisms through which maternal stress during pregnancy is transmitted to the foetuses and the foetal brain is programmed by prenatal stress and the potential to overwrite programming of the offspring are discussed.Reproduction (2013) 146 R175-R189

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“…The fact that a similar concentration of cortisol is associated with different consequences in boys and girls suggests a sex-specific programming effect, i.e., the same environmental cue is not associated with the same outcome in boys and girls. There are several examples in the animal and human literature to suggest many prenatal insults produce outcome-specific sexually dimorphic developmental consequences (33,60,(62)(63)(64). Mechanisms that have been discussed in this context include the presence of sex-specific placental adaptation to stress exposure (65) and the notion of increased susceptibility of the female brain to its milieu given the more rapid neurodevelopmental trajectory in females compared with males (66,67).…”

Section: Discussionmentioning

confidence: 99%

“…Sex. Because many animal and human studies suggest that fetal/child sex may moderate the effects of pre-or postnatal exposures on developmental outcomes (62,63,94), we included an interaction term between maternal prenatal cortisol and sex of the child in all our statistical models (SI Materials and Methods provides further details).…”

Section: Methodsmentioning

confidence: 99%

Maternal cortisol over the course of pregnancy and subsequent child amygdala and hippocampus volumes and affective problems

Buß

Davis²,

Shahbaba³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

534

496

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Stress-related variation in the intrauterine milieu may impact brain development and emergent function, with long-term implications in terms of susceptibility for affective disorders. Studies in animals suggest limbic regions in the developing brain are particularly sensitive to exposure to the stress hormone cortisol. However, the nature, magnitude, and time course of these effects have not yet been adequately characterized in humans. A prospective, longitudinal study was conducted in 65 normal, healthy mother-child dyads to examine the association of maternal cortisol in early, mid-, and late gestation with subsequent measures at approximately 7 y age of child amygdala and hippocampus volume and affective problems. After accounting for the effects of potential confounding pre-and postnatal factors, higher maternal cortisol levels in earlier but not later gestation was associated with a larger right amygdala volume in girls (a 1 SD increase in cortisol was associated with a 6.4% increase in right amygdala volume), but not in boys. Moreover, higher maternal cortisol levels in early gestation was associated with more affective problems in girls, and this association was mediated, in part, by amygdala volume. No association between maternal cortisol in pregnancy and child hippocampus volume was observed in either sex. The current findings represent, to the best of our knowledge, the first report linking maternal stress hormone levels in human pregnancy with subsequent child amygdala volume and affect. The results underscore the importance of the intrauterine environment and suggest the origins of neuropsychiatric disorders may have their foundations early in life.developmental programming | fetal origins | hypothalamus-pituitaryadrenal axis | depression | emotion regulation

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Differential Effect of Prenatal Stress on the Expression of Cortiocotrophin-Releasing Hormone and its Receptors in the Hypothalamus and Amygdala in Male and Female Rats

Cited by 97 publications

References 56 publications

HPA axis genetic variation, pubertal status, and sex interact to predict amygdala and hippocampus responses to negative emotional faces in school-age children

HPA axis genetic variation, pubertal status, and sex interact to predict amygdala and hippocampus responses to negative emotional faces in school-age children

Effects of maternal exposure to social stress during pregnancy: consequences for mother and offspring

Maternal cortisol over the course of pregnancy and subsequent child amygdala and hippocampus volumes and affective problems

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