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Updated: Mar 13, 2026

Using a Murine Model of Psychosocial Stress in Pregnancy as a Translationally Relevant Paradigm for Psychiatric Disorders in Mothers and Infants
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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

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Impact of Maternal Stress in Pregnancy on Brain Function of the Offspring

Jun Udagawa1, Kodai Hino

  • 1Division of Anatomy and Cell Biology, Department of Anatomy, Shiga University of Medical Science.

Nihon Eiseigaku Zasshi. Japanese Journal of Hygiene
|October 12, 2016
PubMed

Insights

Prenatal stress, including malnutrition and maternal immune activation, increases risks for schizophrenia, autism spectrum disorder (ASD), and attention-deficit hyperactivity disorder (ADHD) in offspring. These risks are linked to epigenetic changes and altered stress response pathways.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Psychiatry

Background:

  • Prenatal stress exposure is linked to increased risks of schizophrenia, autism spectrum disorder (ASD), and attention-deficit hyperactivity disorder (ADHD).
  • The first trimester is a critical developmental window where disturbances in neurogenesis and neuronal migration may increase susceptibility to these disorders.
  • Epigenetic modifications, influenced by stress, play a role in gene expression regulation and are implicated in developmental disabilities.

Purpose of the Study:

  • To elucidate the pathophysiological mechanisms linking prenatal stressors to increased risks of schizophrenia, ASD, and ADHD.
  • To explore the role of epigenetic modifications, maternal immune activation (MIA), and the hypothalamic-pituitary-adrenal (HPA) axis in mediating these risks.

Main Methods:

  • Review of epidemiological studies and molecular mechanisms.
  • Investigation of how MIA is induced by stressors like polyinosinic-polycytidylic acid, lipopolysaccharide, high-fat diets, and obesity.
  • Analysis of stress-induced reprogramming of the HPA axis.

Main Results:

  • MIA, induced by various prenatal stressors, leads to neuroinflammation and epigenetic modifications in offspring.
  • Maternal high-fat diet and obesity can also induce MIA, potentially increasing developmental disability risks.
  • Maternal stress alters the offspring's HPA axis, affecting their stress response.

Conclusions:

  • Prenatal stress exposure can increase offspring susceptibility to schizophrenia, ASD, and ADHD.
  • Epigenetic modifications, MIA, and HPA axis alterations are key mechanisms underlying this increased susceptibility.
  • Understanding these mechanisms is crucial for developing preventative strategies for neurodevelopmental disorders.

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