Antenatal glucocorticoids blunt the functioning of the hypothalamic-pituitary-adrenal axis of neonates and disturb some behaviors in juveniles

Burlet, Ghislaine; Fernette, Brigitte; Blanchard, Samra; Angel, E.; Tankosic, P.; Maccari, Stefania; Burlet, Arlette

doi:10.1016/j.neuroscience.2005.01.018

Cited by 38 publications

(26 citation statements)

References 43 publications

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“…However, elevated maternal glucocorticoids during late gestation caused an increase in birth weight of LG-ACTH piglets. Such higher birth weights after prenatal ACTH or stress treatments were described for calves and lambs (Lay et al 1997b, Roussel et al 2004, whereas in rodents and humans, maternal restraint stress or prenatal dexamethasone treatment generally decreases the birth weights (Bloom et al 2001, Lesage et al 2004, Burlet et al 2005. This discrepancy may result from differences in the fetal development as well as species sensitivity to glucocorticoids.…”

Section: Discussionmentioning

confidence: 94%

Changes in endocrine and neurochemical profiles in neonatal pigs prenatally exposed to increased maternal cortisol

Kanitz¹,

Otten²,

Tuchscherer³

2006

Journal of Endocrinology

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Early life environmental factors are able to influence prenatal development and may cause structural and functional effects on hypothalamic-pituitary-adrenal (HPA) axis and neurotransmitter systems in the offspring. These effects seem to be species specific and may depend on the period of gestation when the factors are effective. Elevated maternal cortisol levels are assumed to play a crucial role as a programming factor during prenatal development. Thus, the present study was performed in order to examine the effects of increased maternal cortisol levels during mid-and late gestation on central and peripheral alterations of the HPA axis and brain neurotransmitter profiles in piglets. Endogenous cortisol release was induced by i.m. administration of ACTH to sows every second day either during mid-(day 49 until 75) or late gestation (day 85 until 107). Controls received injections of saline. ACTH treatment of sows during mid-and late gestation had no effects on the gestation length, the number of total born and the frequency of stillborn piglets. However, ACTH treatment during late gestation caused an increase of birth weight (P!0$04) and affected the organ:body weight ratios (brain and adrenal) in the offspring. There was an impact of increased maternal cortisol on the HPA axis and on central neurotransmitter systems in the offspring. ACTH treatment during mid gestation caused a significant decrease of plasma corticosteroid-binding globulin (CBG; P!0$03) and an increase of the noradrenergic activity in the locus coeruleus (LC) region (P!0$02). Elevated maternal cortisol during late gestation also produced a significant decrease of plasma CBG (P!0$05), but significantly increased the plasma noradrenaline (NA) concentration (P!0$02) and decreased the serotonergic activity in the LC at both postnatal day 1 (P!0$016) and day 28 (P!0$003). Furthermore, there were sex-specific effects of ACTH treatment on plasma CBG, NA and brain monoamine turnover, with more pronounced changes in male offspring. In conclusion, elevated maternal cortisol levels during mid-and late gestation in pigs affect growth, HPA axis and brain neurotransmitter systems in the offspring in a sex-specific manner. The observed alterations in endocrine and neurotransmitter systems are dependent on the gestational period. Late gestation appears to be a more sensitive phase for cortisol-induced programming in pigs. Moreover, the present data show that there are marked developmental differences between laboratory animals and domestic pigs, and highlight the importance of speciesspecific studies on prenatal influences.

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Section: Discussionmentioning

confidence: 94%

Changes in endocrine and neurochemical profiles in neonatal pigs prenatally exposed to increased maternal cortisol

Kanitz¹,

Otten²,

Tuchscherer³

2006

Journal of Endocrinology

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“…In rodents prenatal GC treatment blunts the HPA axis response in the offspring during the neonatal period. 15 Furthermore, fetal exposure to GCs leads to lifelong alterations in HPA axis functioning. 16,17 Similarly, sheep and primate studies have demonstrated that a synthetic GC treatment, modeled after the regimen currently given to pregnant women, alters HPA responsiveness in the offspring at up to 1 year of age.…”

Section: Discussionmentioning

confidence: 99%

Antenatal betamethasone treatment has a persisting influence on infant HPA axis regulation

et al. 2006

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Objective: To examine the consequences of antenatal betamethasone (AB) exposure on postnatal stress regulation.Study design: Fourteen AB exposed infants born at 28-30 weeks' gestation were assessed in the NICU during postnatal week 1 and at 34 weeks postconception. Nine infants born at 34 weeks gestation without AB treatment were evaluated as a postconceptional age comparison group. Salivary cortisol, heart rate, and behavior were measured at baseline and in response to a heelstick blood draw.Results: Repeated measures ANOVAs revealed that both groups displayed an increase in heart rate and behavioral distress in response to the stressor. The cortisol response, however, was blunted in AB-treated infants at both assessments.Conclusion: AB treatment has consequences for hypothalamicpituitary-adrenal (HPA) axis regulation that persist for at least four to six weeks after birth, indicating that studies of long-term effects are warranted.

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“…Cumulative neonatal morphine exposure was indexed as the average daily dose of intravenous morphine adjusted for daily weight, multiplied by the number of days of intravenous morphine administration. Knowing that exposure to postnatal glucocorticoids can affect the HPA axis of juvenile offspring (Burlet et al, 2005), we also recorded the number of days of exposure to postnatal glucocorticoids for each preterm infant. Overall, six infants received glucocorticoids postnatally.…”

Section: Infant Measuresmentioning

confidence: 99%

Maternal stress and behavior modulate relationships between neonatal stress, attention, and basal cortisol at 8 months in preterm infants

Grunau

Petrie-Thomas

et al. 2007

Developmental Psychobiology

119

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There is evidence that the developmental trajectory of cortisol secretion in preterm infants is altered, with elevated basal cortisol levels observed postnatally through at least 18 months corrected age (CA). This alteration is possibly due to neonatal pain-related stress. High cortisol levels might contribute to greater risk of impaired neurodevelopment. Since maternal factors are important for the regulation of infant stress responses, we investigated relationships between infant (neonatal painrelated stress, attention, cortisol) and maternal (stress, interactive behaviors) factors at age 8 months CA. We found that interactive maternal behaviors buffered the relationship between high neonatal pain-related stress exposure and poorer focused attention in mothers who self-reported low concurrent stress. Furthermore, in preterm infants exposed to high concurrent maternal stress and overwhelming interactive maternal behaviors, higher basal cortisol levels were associated with poor focused attention. Overall, these findings suggest that maternal factors can influence the cognitive resilience at 8 months of preterm infants exposed to early life stress.

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Antenatal glucocorticoids blunt the functioning of the hypothalamic-pituitary-adrenal axis of neonates and disturb some behaviors in juveniles

Cited by 38 publications

References 43 publications

Changes in endocrine and neurochemical profiles in neonatal pigs prenatally exposed to increased maternal cortisol

Changes in endocrine and neurochemical profiles in neonatal pigs prenatally exposed to increased maternal cortisol

Antenatal betamethasone treatment has a persisting influence on infant HPA axis regulation

Maternal stress and behavior modulate relationships between neonatal stress, attention, and basal cortisol at 8 months in preterm infants

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