Répétition des cures de corticoïdes chez les femmes à risque d’accouchement prématuré : un consensus difficile

Guilherme, Romain; Renaud, Claire; Dommergues, Marc; Mitanchez, Delphine

doi:10.1016/j.jgyn.2008.12.004

Cited by 4 publications

(1 citation statement)

References 60 publications

(75 reference statements)

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“…These treatments are performed despite evidence that they retard growth and dramatically reduce body weight (Seckl, 2001). Infants treated with DEX, both preterm or following preterm delivery, show detriments in cognitive and motor development as well as disrupted hypothalamic-pituitary-adrenal (HPA) axis function (Barrington, 2001; Jones, 2005; Karemaker et al, 2008; Guilherme et al, 2009). …”

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confidence: 99%

Dexamethasone induces apoptosis in the developing rat amygdala in an age-, region-, and sex-specific manner

et al. 2011

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Exposure to glucocorticoids (GCs) in early development can lead to long-term changes in brain function and behavior although little is known about the underlying neural mechanisms. Perinatal exposure to GCs alters adult anxiety and neuroendocrine responses to stress. Therefore, we investigated the effects of either late gestational or neonatal exposure to the GC receptor agonist dexamethasone (DEX), on apoptosis within the amygdala, a region critical for emotional regulation. DEX was administered to timed-pregnant rat dams from gestational day 18 until parturition, or postnatal day 4-6. Offspring were sacrificed the day following the last DEX treatment and tissue was processed for immunohistochemical detection of cleaved caspase-3, a marker for apoptotic cells. Prenatal DEX treatment significantly increased the number of cleaved caspase-3 positive cells in the amygdala of both sexes, largely due to increases within the medial and basomedial sub-regions. Postnatal DEX treatment also increased cleaved caspase-3 immunoreactivity within the amygdala, although effects reached significance only in the central nucleus of females. Overall, DEX induction of cleaved caspase-3 in the amygdala was greater following prenatal compared to postnatal treatment, yet in both instances elevations in cleaved caspase-3 correlated with an increase in pro-apoptotic Bax mRNA expression. Dual-label immunohistochemistry of cleaved caspase-3 and the neuronal marker NeuN confirmed that virtually all cleaved caspase-3 positive cells in the amygdala were neurons and a subset of these cells (primarily following postnatal treatment) expressed a GABAergic calcium binding protein phenotype (calbindin or calretinin). Together these results indicate that early developmental GC exposure induces neuronal apoptosis within the amygdala in an age, sex, and region dependent manner.

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confidence: 99%

Dexamethasone induces apoptosis in the developing rat amygdala in an age-, region-, and sex-specific manner

et al. 2011

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Perinatal dexamethasone‐induced alterations in apoptosis within the hippocampus and paraventricular nucleus of the hypothalamus are influenced by age and sex

Zuloaga

Carbone

Quihuis

et al. 2012

J of Neuroscience Research

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Exposure to high levels of glucocorticoids (GCs) during development leads to long-term changes in hypothalamic-pituitary-adrenal (HPA) axis regulation, although little is known about the neural mechanisms that underlie these alterations. In this study, we investigated the effects of late gestational (days 18-22) or postnatal (days 4-6) administration of the GC receptor agonist dexamethasone (DEX) on an apoptosis marker in two brain regions critical to HPA axis regulation, the hippocampus and the hypothalamic paraventricular nucleus (PVN). One day after the final DEX injection, male and female rats were sacrificed, and brains were processed for immunohistochemical detection of cleaved caspase-3, an apoptotic cell death indicator. DEX increased cleaved caspase-3 immunoreactivity in the CA1 hippocampal region of both sexes following prenatal but not postnatal treatment. Prenatal DEX also increased caspase-3 immunoreactivity in the CA3 region, an elevation that tended to be greater in females. In contrast, postnatal DEX resulted in a much smaller, albeit significant, induction in CA3 caspase-3 compared with prenatal treatment. Quantitative real-time PCR analysis revealed that prenatal but not postnatal DEX-induced hippocampal cleaved caspase-3 correlated with elevated mRNA of the proapoptotic gene Bad. Few caspase-3-ir cells were identified within the PVN regardless of treatment age, although postnatal but not prenatal DEX increased this number. However, the region immediately surrounding the PVN (peri-PVN) showed significant increases in caspase-3-ir cells following pre- and postnatal DEX. Together these findings indicate that developmental GC exposure increases apoptosis in HPAaxis-associated brain regions in an age- and sex-dependent manner.

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Frühgeburt und Amnioninfektionssyndrom

Tucher¹,

Henrich²

2013

Therapiehandbuch Gynäkologie Und Geburtshilfe

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Répétition des cures de corticoïdes chez les femmes à risque d’accouchement prématuré : un consensus difficile

Cited by 4 publications

References 60 publications

Dexamethasone induces apoptosis in the developing rat amygdala in an age-, region-, and sex-specific manner

Dexamethasone induces apoptosis in the developing rat amygdala in an age-, region-, and sex-specific manner

Perinatal dexamethasone‐induced alterations in apoptosis within the hippocampus and paraventricular nucleus of the hypothalamus are influenced by age and sex

Frühgeburt und Amnioninfektionssyndrom

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