Maternal Stress, HPA Activity, and Fetal/Infant Outcome<sup>a</sup>

Sandman, Curt A.; Wadhwa, Pathik D.; Chicz-DeMet, Aleksandra; Dunkel-Schetter, Christine; Porto, Manuel

doi:10.1111/j.1749-6632.1997.tb46162.x

Cited by 219 publications

(138 citation statements)

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“…The rapidly lowering CRH level observed involves probably only CRH from the placenta, not from the hypothalamus. Maternal stress during the last weeks of pregnancy may influence the birth outcome (24), but, due to the elevated concentration of placental CRH, it is obviously difficult to estimate the changes in the functioning of the maternal HPA axis and the mother's hypothalamus secretion. In the group of women delivered spontaneously, we hypothesize that the elevation of ACTH levels, moderate but statistically significant, was due to the central regulation of the maternal hypothalamo±pituitary axis by the hypothalamic response to stress.…”

Section: Discussionmentioning

confidence: 99%

Corticotrophin-releasing hormone and ACTH levels in maternal and fetal blood during spontaneous and oxytocin-induced labour

et al. 2001

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The changes in corticotrophin-releasing hormone (CRH), ACTH and dehydroepiandrosterone (DHEA) in maternal and fetal plasma were estimated in women undergoing spontaneous and oxytocininduced labour to correlate hormone changes with the mode of parturition. Blood was sampled from a maternal peripheral vein 2 days before labour, during the second stage of labour and on the second postnatal day, and also from umbilical vessels just after delivery. Hormone concentrations were measured by RIA and ELSA methods. The maternal plasma CRH concentration before labour was significantly higher in the group of women delivered spontaneously and declined during the labour through to the second postnatal day. Measured in umbilical vessels, CRH as well as ACTH concentrations were higher in the umbilical vein than artery. The mean maternal plasma ACTH was similar in both groups before delivery, then increased significantly in both groups during the labour, decreasing on the second day after delivery. There were no changes in DHEA concentrations among the groups and at all time points of collection. No correlations between CRH and ACTH or DHEA were observed. Our results suggest that the maternal pituitary can respond to stress factors during delivery but peripheral CRH, probably mainly of placental origin, is not a major modulator of pituitary action.

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Section: Discussionmentioning

confidence: 99%

Corticotrophin-releasing hormone and ACTH levels in maternal and fetal blood during spontaneous and oxytocin-induced labour

et al. 2001

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“…Given that hypoxia and nutrient restriction activate the foetal HPA axis (Edwards & McMillen 2002, Roelfsema et al 2005) and elicit foetal sympathetic-adrenomedullary stress responses (Gu & Jones 1986), these responses may contribute to the foetal programming of HPA axis responsivity and anxiety-like behaviour in the adult offspring , Lingas & Matthews 2001, Nunez et al 2008, Fan et al 2009, Wang et al 2013. The adrenal medulla also secretes b-endorphin following stress exposure, which may cross the placenta to influence the development of the foetal brain (Sandman et al 1997).…”

Section: Role For Catecholamines?mentioning

confidence: 99%

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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“…Animal models for chronic, psychological stress early in life 7.1. The timing of suitable chronic stress modelsThe critical period of vulnerability to early-life experience, including stress, in humans is difficult to determine, and likely includes both late gestation and early infancy [124,7]. In the rat, the critical developmental period for stress-related hippocampal plasticity is better understood.…”

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confidence: 99%

Hippocampal neuroplasticity induced by early-life stress: Functional and molecular aspects

Fenoglio¹,

Brunson²,

Baram³

2006

Frontiers in Neuroendocrinology

189

138

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Whereas genetic factors contribute crucially to brain function, early-life events, including stress, exert long-lasting influence on neuronal function. Here, we focus on the hippocampus as the target of these early-life events because of its crucial role in learning and memory. Using a novel immaturerodent model, we describe the deleterious consequences of chronic early-life 'psychological' stress on hippocampus-dependent cognitive tasks. We review the cellular mechanisms involved and discuss the roles of stress-mediating molecules, including corticotropin releasing hormone, in the process by which stress impacts the structure and function of hippocampal neurons. KeywordsNeonatal; Rat; Human; Stress; Memory; Hippocampus; Corticotropin releasing hormone; CRF; Hypothalamic pituitary adrenal axis; Neuroplasticity Early-life events interact with genetic factors to influence hippocampal function long-termBrain function and dysfunction throughout life are determined by the interaction of genetic factors with 'acquired' environmental events, signals and stimuli [100]. Events that occur early in life are capable of exerting effects that persist throughout adulthood. Here, we focus on the hippocampus as the target of these early-life events because of its crucial role in learning, memory storage and retrieval, and general cognitive function [105,41,65]. Indeed, early-life events, via complex interactions with genetic factors [106,120], have been suspected to be a major determinant of smaller hippocampal volume and long-term cognitive dysfunction in preterm infants [111,17] and may play a role in certain affective and dementing disorders in the adult and aging human [100,26,120]. This review focuses on the mechanisms by which certain early-life events influence populations of hippocampal neurons acutely, and impact the function and integrity of the hippocampus long-term. Studying early-life stress may be used to probe the molecular mechanisms involved in experience-evoked hippocampal neuroplasticityStress may provide a salient example of early-life experience that might exert long-lasting influence on the brain, because (1) over 50% of the world's children are exposed to stress [139] and (2) evidence from both human and animal studies suggests that early-life stress has profound effects on cognitive function and emotional health.Stress has been shown to influence the hippocampus in a number of important ways. Whereas acute mild stress rapidly enhances synaptic efficacy and learning and memory processes [131,45,91,123], chronic or severe activation of the stress response early in life has been shown to be potentially injurious in both humans [6,120,147] and experimental animals [120,31]. For example, severe childhood psychological stress (neglect and abuse) correlates with a higher incidence of learning disabilities later in life, including those learning and memory functions requiring an intact hippocampus [121,50]. Further, MRI studies have suggested that adults subjected to abuse (a measure of chronic stress) ...

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Maternal Stress, HPA Activity, and Fetal/Infant Outcome^a

Cited by 219 publications

References 35 publications

Corticotrophin-releasing hormone and ACTH levels in maternal and fetal blood during spontaneous and oxytocin-induced labour

Corticotrophin-releasing hormone and ACTH levels in maternal and fetal blood during spontaneous and oxytocin-induced labour

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

Hippocampal neuroplasticity induced by early-life stress: Functional and molecular aspects

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Maternal Stress, HPA Activity, and Fetal/Infant Outcomea

Cited by 219 publications

References 35 publications

Corticotrophin-releasing hormone and ACTH levels in maternal and fetal blood during spontaneous and oxytocin-induced labour

Corticotrophin-releasing hormone and ACTH levels in maternal and fetal blood during spontaneous and oxytocin-induced labour

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

Hippocampal neuroplasticity induced by early-life stress: Functional and molecular aspects

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Maternal Stress, HPA Activity, and Fetal/Infant Outcome^a