Glucocorticoids, prenatal stress and the programming of disease

Harris, Anjanette; Seckl, Jonathan R.

doi:10.1016/j.yhbeh.2010.06.007

Cited by 705 publications

(629 citation statements)

References 202 publications

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Section: Glucocorticoidsmentioning

confidence: 99%

“…Nonetheless, other factors such as cytokines (e.g., IL-1β and IL-6) also modulate GC responses to stressors in the hippocampus, hypothalamus, and pituitary [72,73] . In fact, cellular studies have shown that the activation of cytokine-dependent signal transduction pathways by pro-infl ammatory cytokines contributes to the GC-dependent deregulation of the HPA axis and to the altered feedback regulation of CRH and AVP peptides in the hypothalamus as well [74,75] .Interestingly, antidepressant treatment has been extensively reported to restore the normal activity of the HPA axis and to improve the inhibitory negative feedback responses of target tissues to GCs. These observations led some authors to suggest that the HPA axis might be the final common pathway that drives most of the symptomatology in depressive disorders, as well as several Neurosci Bull June 1, 2015, 31(3): 338-350 342 acute symptoms of other psychiatric disorders [76] .…”

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confidence: 99%

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Hypothalamic-pituitary-adrenal axis function during perinatal depression

et al. 2015

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Abnormal function of the hypothalamic-pituitary-adrenal (HPA) axis is an important pathological finding in pregnant women exhibiting major depressive disorder. They show high levels of cortisol proinflammatory cytokines, hypothalamic-pituitary peptide hormones and catecholamines, along with low dehydroepiandrosterone levels in plasma. During pregnancy, the TH2 balance together with the immune system and placental factors play crucial roles in the development of the fetal allograft to full term. These factors, when altered, may generate a persistent dysfunction of the HPA axis that may lead to an overt transfer of cortisol and toxicity to the fetus at the expense of reduced activity of placental 11β-hydroxysteroid dehydrogenase type 2. Epigenetic modifications also may contribute to the dysregulation of the HPA axis. Affective disorders in pregnant women should be taken seriously, and therapies focused on preventing the deleterious effects of stressors should be implemented to promote the welfare of both mother and baby.Keywords: brain; depression; neuroendocrine; pregnancy; stress; glucocorticoids Extensive studies have demonstrated that early life stressors produce changes in behavior and enhance the sensitivity of the stress response systems [1][2][3][4] . Although the genetic background has been implicated in the development of mood-related disorders, and genetic research has identified some chromosomal regions and genes that are involved in susceptibility to mood disorders, the etiology of anxiety and depressive disorders is still not clear in humans, particularly in women with major depressive disorder (MDD) [1] .The pathogenesis of perinatal depression is an emerging field. Although considerable progress has been made in this area in the last few years, there still remain unanswered questions and gaps in our knowledge of the underlying pathogenesis, the long-term impact of perinatal depression on the developing fetus, and the best methods for counseling pregnant women concerning the risks of untreated MDD versus the risks of psychopharmacologic treatment during pregnancy and lactation [5] . Meta-analysis studies have reported that the mean prevalence rate of prenatal depression is ~12% (this varies greatly according to location, mode of assessment, and socioeconomic conditions), and show that a large percentage of pregnant women displaying major depression remain depressed in the postpartum period and/or continuously [6,7] . Anxiety, depressive disorder, and stress during pregnancy are risk Phillipe Leff Gelman, et al. HPA axis in perinatal depression 339 factors for negative outcomes in newborns, like preterm birth or low birth weight; also, insecure attachment and impaired child development could be a consequence of mental disorders during pregnancy [6,[8][9][10] . The mechanisms by which maternal depression impacts fetal and neonatal development are currently under investigation; there is some evidence that depressive symptoms impact the infant's hypothalamic-pituitary-adrenal (HPA) axis, enhancing the ...

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Section: Glucocorticoidsmentioning

confidence: 99%

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confidence: 99%

Hypothalamic-pituitary-adrenal axis function during perinatal depression

et al. 2015

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“…The most widely exploited hypothesis for the underlying mechanisms states that the fetus is exposed to an excess of maternally derived glucocorticoids when the latter are raised at times of stress. Such fetal exposure underpins alterations in brain development and in the functioning of the hypothalamic-pituitary-adrenal axis (HPA) (Van den Bergh et al, 2005;Cottrell and Seckl, 2009;Harris and Seckl, 2011;Charil et al, 2010;Glover et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Cortisol and anxiety response to a relaxing intervention on pregnant women awaiting amniocentesis

Ventura

Gomes

Carreira

2012

Psychoneuroendocrinology

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“…Importantly, stress-related pathology can be trans-generationally transmitted through epigenetic phenomena and changes in gene expression have been shown to persist long after the initial stress exposure, which may predispose the individual for disease in later life (41). The effects of high maternal stress levels during pregnancy appear to be transmitted to one or two subsequent generations, which may result in an accumulative increase in vulnerability to depression in future generations (42). Since complex gene-environment interactions seem to contribute to the vulnerability to depression, contextual considerations are increasingly relevant from this traditionally more deterministic perspective.…”

Section: Genetic and Epigenetic Mechanismsmentioning

confidence: 99%

The neuroscience and context of adolescent depression

Blom

Connolly

et al. 2016

Acta Paediatrica

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Adolescent depression is a growing public health concern with an increased risk of negative health outcomes, including suicide. The use of antidepressants and psychotherapy has not halted its increasing prevalence and there is a critical need for effective prevention and treatment. We reviewed the neuroscience of adolescent depression, with a focus on the neurocircuitry of sustained threat and summarised contextual factors that have an impact on brain development and the pathophysiology of depression. We also reviewed novel treatment models. Conclusion Attention to the relevant neurocircuitry and contextual factors implicated in adolescent depression is necessary to advance prevention and treatment development.

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Glucocorticoids, prenatal stress and the programming of disease

Cited by 705 publications

References 202 publications

Hypothalamic-pituitary-adrenal axis function during perinatal depression

Hypothalamic-pituitary-adrenal axis function during perinatal depression

Cortisol and anxiety response to a relaxing intervention on pregnant women awaiting amniocentesis

The neuroscience and context of adolescent depression

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