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Updated: Jan 31, 2026

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Microglia activation in the offspring of prenatal Poly I: C exposed rats: a PET imaging and immunohistochemistry

Xue Li1, Xin Tian1, Luxian Lv2,3

  • 1The First Affiliated Hospital/Zhengzhou University, Zhengzhou, China.

General Psychiatry
|December 25, 2018
PubMed
Abstract

Insights

Prenatal exposure to Poly I:C in rats leads to microglia activation and behavioral changes, suggesting a role in schizophrenia pathogenesis. This study quantifies neuroinflammation in offspring using advanced imaging and histology.

Area of Science:

  • Neuroscience
  • Immunology
  • Psychiatry

Background:

  • Maternal viral infection during pregnancy is linked to neurodevelopmental psychiatric disorders like schizophrenia.
  • Microglia, the brain's immune cells, are crucial in neuroinflammation.
  • Polyriboinosinic-polyribocytidilicacid (Poly I:C) exposure in utero serves as a model for prenatal infection.

Purpose of the Study:

  • To quantify microglia activation in vivo in the prefrontal cortex and hippocampus of adult rats exposed to Poly I:C during gestation.
  • To investigate the behavioral outcomes associated with prenatal Poly I:C exposure.

Main Methods:

  • Utilized a rat model with Poly I:C exposure during pregnancy versus saline controls.
  • Assessed behavioral changes using spontaneous activity, prepulse inhibition (PPI), and latent inhibition (LI) tests.
  • Quantified microglia activation using 11C-PK11195 positron emission tomography (PET) and immunohistochemistry.

Main Results:

  • Poly I:C offspring exhibited hyperlocomotion and deficits in PPI and LI.
  • Increased 11C-PK11195 uptake was observed in the prefrontal cortex and hippocampus of the treatment group.
  • Significantly higher numbers of activated microglia were found in the prefrontal cortex and hippocampus of Poly I:C exposed rats.

Conclusions:

  • Prenatal Poly I:C exposure induces microglia activation in the mature offspring's prefrontal cortex and hippocampus.
  • Microglia activation is implicated as a potential factor in the pathogenesis of schizophrenia.
Keywords:
PEThippocampusmicroglianeuroinflammationschizophrenia

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