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.
Abstract

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