Interaction of the pre- and postnatal environment in the maternal immune activation model
Anna Gundacker1, Laura Cuenca Rico1, Peter Stoehrmann1
1Department of Neurophysiology and Neuropharmacology, Center for Physiology and Pharmacology, Medical University of Vienna, Schwarzspanierstrasse, 17, 1090 Vienna, Austria.
Insights
Maternal immune activation during pregnancy can negatively impact offspring neurodevelopment. This review explores how prenatal and postnatal maternal environments interact to influence offspring outcomes, particularly in the context of the maternal immune activation model.
Area of Science:
- Neuroscience
- Developmental Biology
- Immunology
Background:
- Adverse pregnancy influences, including stress, infection, and nutritional imbalance, are linked to offspring neurodevelopmental issues.
- The maternal immune activation (MIA) model is crucial for studying how maternal immune stimulation during gestation affects fetal neurodevelopment.
- MIA can lead to behavioral and cognitive abnormalities in offspring, often explained by the 'double-hit hypothesis'.
Purpose of the Study:
- To review the interaction between prenatal and postnatal maternal environments in modulating offspring development.
- To examine the relevance of these interactions within the pathophysiology of the MIA model.
- To understand how MIA impacts maternal brain function and postpartum behavior, contributing to offspring neurodevelopmental consequences.
Main Methods:
- Review of preclinical research utilizing the maternal immune activation (MIA) model.
- Analysis of studies investigating the effects of prenatal environmental insults on offspring neurodevelopment.
- Examination of research on the impact of the postnatal maternal environment on offspring outcomes.
Main Results:
- Maternal immune activation during gestation disrupts fetal neurodevelopment, leading to later-life behavioral and cognitive deficits in offspring.
- The 'double-hit hypothesis' suggests that cumulative environmental adversities increase the risk for neurodevelopmental disorders.
- MIA affects the maternal brain, potentially altering postpartum behavior and further impacting progeny.
Conclusions:
- The interplay between prenatal and postnatal maternal environments significantly modulates offspring neurodevelopment.
- Understanding these interactions is critical for comprehending the long-term consequences of MIA.
- Targeting both prenatal and postnatal maternal factors may be essential for mitigating neurodevelopmental risks in offspring.
Abstract:
Adverse influences during pregnancy are associated with a range of unfavorable outcomes for the developing offspring. Maternal psychosocial stress, exposure to infections and nutritional imbalances are known risk factors for neurodevelopmental derangements and according psychiatric and neurological manifestations later in offspring life. In this context, the maternal immune activation (MIA) model has been extensively used in preclinical research to study how stimulation of the maternal immune system during gestation derails the tightly coordinated sequence of fetal neurodevelopment. The ensuing consequence of MIA for offspring brain structure and function are majorly manifested in behavioral and cognitive abnormalities, phenotypically presenting during the periods of adolescence and adulthood. These observations have been interpreted within the framework of the "double-hit-hypothesis" suggesting that an elevated risk for neurodevelopmental disorders results from an individual being subjected to two adverse environmental influences at distinct periods of life, jointly leading to the emergence of pathology. The early postnatal period, during which the caregiving parent is the major determinant of the newborn´s environment, constitutes a window of vulnerability to external stimuli. Considering that MIA not only affects the developing fetus, but also impinges on the mother´s brain, which is in a state of heightened malleability during pregnancy, the impact of MIA on maternal brain function and behavior postpartum may importantly contribute to the detrimental consequences for her progeny. Here we review current information on the interaction between the prenatal and postnatal maternal environments in the modulation of offspring development and their relevance for the pathophysiology of the MIA model.
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