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Using a Murine Model of Psychosocial Stress in Pregnancy as a Translationally Relevant Paradigm for Psychiatric Disorders in Mothers and Infants
Published on: June 13, 2021
Glucocorticoids as Mediators of Adverse Outcomes of Prenatal Stress
Anthi C Krontira1, Cristiana Cruceanu2, Elisabeth B Binder2
1Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany; International Max Planck Research School for Translational Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.
Insights
Prenatal stress can alter fetal development, leading to lasting behavioral and physiological changes in offspring. Understanding how prenatal glucocorticoids impact fetal development is key to preventing adverse outcomes.
Area of Science:
- Neuroscience
- Developmental Biology
- Endocrinology
Background:
- Prenatal experiences significantly influence offspring health, with prenatal stress linked to adverse outcomes like cardiovascular and psychiatric conditions.
- Prenatal stress induces neurodevelopmental alterations, manifesting as behavioral changes (e.g., increased fearfulness) and physiological changes (e.g., brain structure/function alterations).
Purpose of the Study:
- To review the mechanisms by which prenatal glucocorticoids mediate the lasting effects of prenatal stress on offspring.
- To explore the impact of prenatal glucocorticoids on the fetal hypothalamic-pituitary-adrenal (HPA) axis, neurodevelopment, and epigenetics.
- To highlight the interplay between these prenatal factors and the offspring's genetic makeup.
Main Methods:
- Literature review focusing on the effects of prenatal glucocorticoids.
- Analysis of studies investigating fetal HPA axis activity, neurodevelopmental processes, and epigenetic modifications.
- Synthesis of research on gene-environment interactions in the context of prenatal stress.
Main Results:
- Elevated prenatal glucocorticoid signaling is a key mediator of prenatal stress effects on offspring.
- Prenatal glucocorticoids can disrupt fetal HPA axis regulation, neurodevelopment, and alter the fetal epigenetic landscape.
- The offspring's genetic background significantly interacts with prenatal glucocorticoid exposure to shape long-term outcomes.
Conclusions:
- Prenatal stress-induced alterations in glucocorticoid signaling represent a critical pathway for long-term adverse outcomes in offspring.
- Understanding these mechanisms, including neurodevelopmental and epigenetic changes, is crucial for developing preventative strategies.
- Future research should consider the interaction between prenatal exposures and offspring genetics to fully elucidate these effects.
Abstract:
A number of prenatal experiences are associated with adverse outcomes after birth, ranging from cardiovascular problems to psychiatric disease. Prenatal stress is associated with neurodevelopmental alterations that persist after birth and manifest at the behavioral level, for example, increased fearfulness, and at the physiological one, that is, brain structural and functional changes. Understanding the mechanisms that drive these lasting effects may help in preventing long-term negative outcomes of prenatal stress. Elevated glucocorticoid signaling in utero may be one of the key mediators of prenatal stress effects on the offspring. In this review, we summarize how prenatal glucocorticoids may impact the activity of the fetal hypothalamic-pituitary-adrenal (HPA) axis, disrupt neurodevelopmental processes and alter the epigenetic landscape of the fetus. We also discuss the need to take into consideration the interaction of these processes with the offspring's genetic landscape.
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