Abstract

Prenatal maternal infection is associated with an increased risk of various neurodevelopmental disorders, including autism spectrum disorders (ASD). Maternal immune activation (MIA) can be experimentally induced by prenatal administration of polyinosinic:polycytidylic acid (poly I:C), a synthetic viral-like double-stranded RNA. Although this MIA model is adopted in many studies, social and communicative deficits, included in the first diagnostic criterion of ASD, are poorly described in the offspring of poly(I:C)-exposed dams. This study aimed to characterize the impact of prenatal poly(I:C) exposure on socio-communicative behaviors in adolescent rats. For this purpose, social play behavior was assessed in both males and females. We also analyzed quantitative and structural changes in ultrasonic vocalizations (USVs) emitted by rats during the play test. Deficits of social play behaviors were evident only in male rats. Males also emitted a significantly decreased number of USVs during social encounters. Prenatal poly(I:C) exposure also affected acoustic call parameters, as reflected by the increased peak frequencies. Additionally, repetitive behaviors were demonstrated in autistic-like animals regardless of sex. This study demonstrates that prenatal poly(I:C) exposure impairs socio-communicative functioning in adolescent rats. USVs may be a useful tool for identifying early autistic-like abnormalities.

Highlights

  • Environmental conditions during prenatal life can influence fetal brain development

  • One of the most frequently applied experimental maternal immune activation (MIA) protocols is based on prenatal exposure of pregnant dams to polyinosinic:polycytidylic acid (poly(I:C)) [4]

  • This study demonstrates that prenatal poly(I:C) exposure impairs socio-communicative functioning in adolescent rats

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Summary

Introduction

One of the most well-known factors linked to neurodevelopmental disorders is infection [1]. Plenty of studies and meta-analyses of human data have shown that maternal infection increases the risk of neuropsychiatric disorders in children [2]. The neurodevelopmental consequences of maternal immune activation (MIA) have been confirmed in animal models [3]. One of the most frequently applied experimental MIA protocols is based on prenatal exposure of pregnant dams to polyinosinic:polycytidylic acid (poly(I:C)) [4]. Poly(I:C) is a synthetic analog of double-stranded RNA that mimics a viral infection. This MIA-based model has been widely used to explore the biochemical, neuroanatomical, and behavioral aspects of neuropsychiatric conditions such as autism spectrum disorders (ASD) [5]

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