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Prenatal stress effects on offspring brain and behavior: Mediators, alterations and dysregulated epigenetic
Shams Ul Haq1, Unis Ahmad Bhat, Arvind Kumar
1CSIR- Centre for Cellular and Molecular Biology (CCMB), Uppal Road, Hyderabad 500 007, India.
Insights
Adverse prenatal conditions, including maternal stress, can alter fetal brain development, leading to lifelong health issues and increased risk for neuropsychiatric disorders in offspring. Key mediators like cortisol play a crucial role in this developmental programming.
Area of Science:
- Neuroscience
- Developmental Biology
- Psychiatry
Background:
- Prenatal environmental factors significantly impact mammalian fetal development.
- Adverse in utero conditions are linked to long-term health consequences for offspring.
- Prenatal stress is a known risk factor for neuropsychiatric disorders.
Purpose of the Study:
- To review the mediators involved in stress transfer from mother to fetus.
- To examine the role of these mediators in fetal programming.
- To detail the brain alterations resulting from prenatal stress and their impact on offspring.
Main Methods:
- Review of existing literature on prenatal stress and fetal development.
- Analysis of mediators such as cortisol, serotonin, cytokines, ROS, and maternal microbiota.
- Focus on molecular, cellular, and structural brain changes in offspring.
Main Results:
- Prenatal stress involves multiple mediators, with cortisol being a primary one.
- Prenatal stress induces alterations in the offspring brain at molecular, cellular, and structural levels.
- These changes result in lasting phenotypic alterations, including behavioral and cognitive deficits.
Conclusions:
- Prenatal stress significantly impacts fetal development, programming offspring for lifelong health risks.
- Mediators like cortisol, serotonin, cytokines, ROS, and maternal microbiota are key in this process.
- Epigenetic mechanisms are central to how prenatal stress affects neural gene expression and brain development.
Abstract:
Prenatal environment significantly influences mammalian fetal development and adverse in utero conditions have life-long consequences for the offspring health. Research has revealed that a wide variety of prenatal stress factors lead to increased risk of vulnerability to neuropsychiatric disorders in the individuals. Multiple mediators are involved in stress transfer from mother to the developing fetus, with stress hormone cortisol being a chief player. Further, the developmental programming effects of prenatal stress have been observed in the form of alterations in the offspring brain at different levels. This review covers stress transfer mediators such as cortisol, serotonin, maternal cytokines, reactive oxygen species (ROS) and the maternal microbiota, and their role in fetal programming. Prenatal stress leads to alterations in the offspring brain at multiple levels, from molecular and cellular to structural. These alterations eventually result in lasting phenotypic alterations such as in the offspring behavior and cognition. Different brain alterations induced by prenatal stress such as in neural pruning processes, neural circuit formation, brain structural connectivity and epigenetic systems regulating neural gene expression are under focus in the second part of the review. The latter constitutes a key molecular mechanism involved in prenatal stress effects and has been discussed in more detail.
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