Maternal viral infection during pregnancy impairs development of fetal serotonergic neurons

Abstract 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...

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Bibliographic Details
Published in:Brain & development (Tokyo. 1979) 2015-01, Vol.37 (1), p.88-93
Main Authors: Ohkawara, Takeshi, Katsuyama, Takashi, Ida-Eto, Michiru, Narita, Naoko, Narita, Masaaki
Format: Article
Language:English
Subjects:
Animals
Autism
Brain - pathology
Chromatography, High Pressure Liquid
Disease Models, Animal
Female
Fetus
In Situ Hybridization
Maternal viral infection
Neurology
Poly I-C - toxicity
Poly I:C
Pregnancy
Pregnancy Complications, Infectious - pathology
Prenatal Exposure Delayed Effects - pathology
Rats
Rats, Wistar
Real-Time Polymerase Chain Reaction
Reverse Transcriptase Polymerase Chain Reaction
Serotonergic Neurons - pathology
Serotonin
Virus Diseases - complications
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Summary:Abstract 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.
ISSN:0387-7604
1872-7131
DOI:10.1016/j.braindev.2014.03.007