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Updated: Apr 30, 2026

Induction of Maternal Immune Activation in Mice at Mid-gestation Stage with Viral Mimic PolyI:C
Published on: March 25, 2016
Maternal viral infection during pregnancy impairs development of fetal serotonergic neurons
Takeshi Ohkawara1, Takashi Katsuyama1, Michiru Ida-Eto1
1Department of Developmental and Regenerative Medicine, Mie University, Graduate School of Medicine, Mie, Japan.
Insights
Maternal viral infection during pregnancy alters fetal development. This study shows poly I:C induced changes in fetal serotonin neuron development and offspring serotonin levels, suggesting a link to neurodevelopmental disorders.
Area of Science:
- Neuroscience
- Developmental Biology
- Immunology
Background:
- Maternal viral infections during pregnancy can cause fetal abnormalities and offspring psychological issues.
- Prenatal exposure to certain chemicals, like thalidomide, can lead to autistic-like phenotypes.
- Prenatal events impacting serotonergic development may cause developmental disorders.
Purpose of the Study:
- To investigate if prenatal viral infection alters neurotransmitter expression in offspring.
- To examine the effects of polyriboinosinic:polyribocytidylic acid (poly I:C) on fetal development and offspring neurochemistry.
Main Methods:
- Administration of poly I:C (a synthetic double-stranded RNA) to pregnant rats on gestational day 9.
- Quantification of serotonin-immunopositive cells on gestational day 15.
- Measurement of hippocampal serotonin content in offspring by postnatal day 50 using high-performance liquid chromatography.
Main Results:
- A 11.1% increase in the number of serotonin-immunopositive neurons was observed in the poly I:C group on gestational day 15.
- A significant decrease in hippocampal serotonin content was found in offspring by postnatal day 50 following poly I:C administration.
Conclusions:
- Maternal viral infection may induce serotonin-related pathogenesis, including neurodevelopmental disorders like autism spectrum disorders.
- Serotonin plays a crucial role in linking prenatal events to postnatal behavior and emotion.
- Prenatal viral infection can contribute to both morphological abnormalities and neurodevelopmental issues in offspring.
Background:
Maternal viral infection during pregnancy induces morphological abnormalities in the fetus and may cause emotional and psychological problems in offspring through unknown mechanisms. We have previously shown that prenatal exposure of rats to chemicals such as thalidomide causes an autistic-like phenotype in offspring, indicating that prenatal events affecting serotonergic development may cause developmental disorder.
Methods:
We investigated whether prenatal viral infection altered the expression of neurotransmitters involved in the emotional or psychological status of offspring. We here took advantage of the polyriboinosinic:polyribocytidylic acid (poly I:C) system, the synthetic double-stranded RNA, which is often used in animal models of viral infection.
Results:
Ten mg/kg of poly I:C was intraperitoneally injected on gestational day (GD) 9 and counted the numbers of serotonin-immunopositive cells on GD15 using flat whole-mount preparation method, resulting 11.1% of increase in the number of serotonergic neurons in poly I:C group. Furthermore, there was a significant decrease in hippocampal serotonin content in offspring by postnatal day 50 following poly I:C administration by high-performance liquid chromatography.
Discussion And Conclusion:
Since serotonin is known to link with behavior and emotion after birth, these results suggest that maternal viral infection might cause, in addition to morphological abnormalities, serotonin-related pathogenesis such as neurodevelopmental disorders including autism spectrum disorders.
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