Prenatal stress and long-term consequences: implications of glucocorticoid hormones

Maccari, Stefania; Darnaudéry, Muriel; Morley‐Fletcher, Sara; Zuena, Anna Rita; Cinque, Carlo; Reeth, Olivier Van

doi:10.1016/s0149-7634(03)00014-9

Cited by 471 publications

(312 citation statements)

References 81 publications

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“…Our results reinforce the fact that brain development is among the processes most vulnerable to glucocorticoids, with disruption of cell acquisition and differentiation achieved at concentrations well below those required for therapeutic interventions. The demonstration of these actions in neural cell cultures, reproducing all the essential findings from glucocorticoid treatment in vivo (Bohn, 1984;Fuxe et al, 1994Fuxe et al, , 1996Gilad et al, 1998;Gould et al, 1997;Kreider et al, 2005aKreider et al, , b, 2006Maccari et al, 2003;Matthews, 2000;Matthews et al, 2002;McEwen, 1992;Meaney et al, 1996;Weinstock, 2001;Welberg and Seckl, 2001), indicates that disrupted neurodevelopment is a direct glucocorticoid effect, not secondary to growth impairment, neuroendocrine disruption or other confounding actions in the fetus, neonate or mother. The successful prevention of respiratory distress in tens of thousands of preterm infants annually in the USA needs to be balanced against the adverse effects on brain development in the hundreds of thousands of individuals that receive the treatment.…”

Section: Discussionmentioning

confidence: 69%

“…First, glucocorticoid use in preterm labor could contribute directly to adverse neurobehavioral outcomes, over and above the confounds of preterm delivery or of secondary effects on the maternalfetal unit, maternal-neonatal interactions, or maternal or offspring neuroendocrine function. Second, the wide window of vulnerability of neurodevelopment to disruption by DEX means that adverse effects, such as those already noted for glucocorticoid administration in vivo (Bohn, 1984;Fuxe et al, 1994Fuxe et al, , 1996Gilad et al, 1998;Gould et al, 1997;Kreider et al, 2005aKreider et al, , b, 2006Maccari et al, 2003;Matthews, 2000;Matthews et al, 2002;McEwen, 1992;Meaney et al, 1996;Weinstock, 2001;Welberg and Seckl, 2001), are likely to be exerted at any stage in the period of 24-34 weeks of gestation in which these agents are recommended for use (Gilstrap et al, 1995). Third, the targeting of multiple stages of neurodevelopment means that the net outcome will differ according to the maturational timetable for neurogenesis and differentiation in each brain region (Bayer et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

“…By themselves, glucocorticoids administered during development can lead to persistent stunting of somatic growth, outright cerebral atrophy, and endocrine disruption, along with a host of behavioral anomalies (Bohn, 1984;Fuxe et al, 1994Fuxe et al, , 1996Gilad et al, 1998;Gould et al, 1997;Maccari et al, 2003;Matthews, 2000;Matthews et al, 2002;McEwen, 1992;Meaney et al, 1996;Weinstock, 2001;Welberg and Seckl, 2001). Nevertheless, most of the animal literature concerns doses of glucocorticoids well above those in clinical use and/or encompass prolonged exposure periods or periods outside the neurodeve-lopmental stages appropriate to mimic the use in humans.…”

Section: Introductionmentioning

confidence: 99%

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Adverse Neurodevelopmental Effects of Dexamethasone Modeled in PC12 Cells: Identifying the Critical Stages and Concentration Thresholds for the Targeting of Cell Acquisition, Differentiation and Viability

Jameson

Seidler

Qiao

et al. 2005

Neuropsychopharmacol

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The use of dexamethasone (DEX) to prevent respiratory distress in preterm infants is suspected to produce neurobehavioral deficits. We used PC12 cells to model the effects of DEX on different stages of neuronal development, utilizing exposures from 24 h up to 11 days and concentrations from 0.01 to 10 mM, simulating subtherapeutic, therapeutic, and high-dose regimens. In undifferentiated cells, even at the lowest concentration, DEX inhibited DNA synthesis and produced a progressive deficit in the number of cells as evaluated by DNA content, whereas cell growth (evaluated by the total protein to DNA ratio) and cell viability (Trypan blue exclusion) were promoted. When cell differentiation was initiated with nerve growth factor, the simultaneous inclusion of DEX still produced a progressive deficit in cell numbers and promoted cell growth and viability while retarding the development of neuritic projections as monitored by the membrane/total protein ratio. Again, even 0.01 mM DEX was effective. We next assessed effects at mid-differentiation by introducing nerve growth factor for 4 days followed by coexposure to DEX. Although effects on cell number, growth, and neurite extension were still detectable, the outcomes were generally less notable. DEX also shifted the fate of PC12 cells away from the cholinergic phenotype and toward the adrenergic phenotype, with the maximum effect achieved at the outset of differentiation. Our results indicate that DEX directly disrupts neuronal cell replication, differentiation, and phenotype at concentrations below those required for the therapy of preterm infants, providing a mechanistic link between glucocorticoid use and neurodevelopmental sequelae.

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Section: Discussionmentioning

confidence: 69%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Adverse Neurodevelopmental Effects of Dexamethasone Modeled in PC12 Cells: Identifying the Critical Stages and Concentration Thresholds for the Targeting of Cell Acquisition, Differentiation and Viability

Jameson

Seidler

Qiao

et al. 2005

Neuropsychopharmacol

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“…We did not have sufficient data to link specific symptoms to individual biological or psychosocial factors, but previous research suggests several targets for further study. A natural target for further research is oestrogen and progesterone, which have neuroregulatory effects, including on the central serotonin system (Moses-Kolko et al 2008), and have been implicated in psychological symptoms in the perinatal period (Maccaria et al 2003;Bloch et al 2003). Also, Fan et al (2009) found that rates of anxiety and depression were higher in the first trimester than later in pregnancy and that depression was correlated with changes in estradiol and progesterone level, and anxiety was correlated with total cortisol level.…”

Section: Discussionmentioning

confidence: 99%

Associated symptoms of depression: patterns of change during pregnancy

Castro

Anderman

Glover

et al. 2017

Arch Womens Ment Health

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Little is known about the natural course of depressive symptoms and associated features throughout pregnancy. We examined the course of some psychological and somatic symptoms in each month of pregnancy in a normative sample. A consecutive, unselected sample of women (N = 374) were interviewed retrospectively at 6 weeks postpartum with the Structured Clinical Interview (DSM-IV). Women were asked whether they had experienced each symptom at any time during pregnancy and the occurrence of the symptom for each month of pregnancy. Associated symptoms of depression showed complex changes across pregnancy. Depressed mood (F(df) = 5.15(1); p = 0.02) showed a quadratic pattern with elevations at the beginning and end of pregnancy. Both linear increases ( a ) and quadratic ( b ) changes over time were observed for sensitivity to criticism (F a (df) = 20.9(1), p a = 0.00; F b (df) = 7.02(1), p b = 0.00), lack of concentration (F a (df) = 37.0(1), p a = 0.00; F b (df) = 10.3(1); p b = 0.00), decreased energy (F a (df) = 13.4(1); p a = 0.00; F b (df) = 62.6(1); p b = 0.00) and feelings of heavy limbs (F a (df) = 92.9(1); p a = 0.00; F b (df) = 67.7(1); p b = 0.00). Only guilt (F(df) = 0.00(1); p = 0.93) showed no significant change over pregnancy. Psychological symptoms changed throughout pregnancy as much as somatic symptoms. A linear increase was found for most symptoms, but significant non-linear changes were also found. The discrepancy between the patterns of depressed mood and most somatic and psychological symptoms suggest complex interactions and potentially important implications for assessment and monitoring treatment.

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“…Developmental conditions can have significant effects on adult morphology, behavior, and physiology [26,4,28,10]. U ltimately, conditions experienced during development may impact growth, recruitment, reproduction, or survival that may in turn affect individual fitness and, perhaps, result in population changes [40,8,27,4,22].…”

Section: Introductionmentioning

confidence: 99%

Effects of developmental conditions on nestling American Kestrel (Falco sparverius) corticosterone concentrations

Strasser

Heath

2011

General and Comparative Endocrinology

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This is an author-produced, peer-reviewed version of this article. AbstractHow nestling birds respond to stressful situations may constitute an important survival component that has lasting developmental effects on the hypothalamic pituitary adrenal (HPA) axis. As birds are exposed to increasing amounts of potential anthropogenic stressors through land use change, understanding how these factors contribute to HPA development is important. We examined whether conditions experienced during the nestling stage affected free-living American Kestrel (Falco sparverius) HPA activity prior to fledging. Kestrels experienced varying levels of human disturbance around their nest and we classified this environmental exposure as high or low environmental human disturbance based on traffic patterns and land use. We then exposed some broods from high and low disturbance areas to a standardized disturbance protocol. Prior to fledging we collected blood samples from 25-day-old nestlings immediately after capture and 15 min post-capture. Corticosterone (CORT) did not vary with environmental human disturbance levels, disturbance protocol treatment, or with an interaction between environmental human disturbance and disturbance protocol treatment suggesting that nestling kestrels may not perceive external conditions related to human disturbance as stressful or kestrels may acclimate to disturbance. We also compared the relative effects of environmental human disturbance outside the nest cavity, conditions within the nest cavity (brood size), and individual condition (nestling fat scores) on baseline and stress-induced CORT. Baseline CORT did not vary with human disturbance level, brood size or fat score. F at scores best explained stress-induced CORT with nestlings in better condition displaying elevated CORT. These results suggest that individual variation is more likely to explain HPA development compared to nest conditions or the external environment. This study demonstrates the importance of considering the effects of developmental conditions on the stress response at several scales.

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Prenatal stress and long-term consequences: implications of glucocorticoid hormones

Cited by 471 publications

References 81 publications

Adverse Neurodevelopmental Effects of Dexamethasone Modeled in PC12 Cells: Identifying the Critical Stages and Concentration Thresholds for the Targeting of Cell Acquisition, Differentiation and Viability

Adverse Neurodevelopmental Effects of Dexamethasone Modeled in PC12 Cells: Identifying the Critical Stages and Concentration Thresholds for the Targeting of Cell Acquisition, Differentiation and Viability

Associated symptoms of depression: patterns of change during pregnancy

Effects of developmental conditions on nestling American Kestrel (Falco sparverius) corticosterone concentrations

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