Microglia, the resident immune cells in the central nervous system, play critical roles in neurodevelopment, synaptic pruning and neuronal wiring. Early in development, microglia migrate via the tangential and radial migration pathways to their final destinations and mature gradually, a process that includes morphological changes. Recent research has implicated microglial abnormality in the etiology of schizophrenia. Since prenatal exposure to viral or bacterial infections due to maternal immune activation (MIA) leads to increased risk of schizophrenia in offspring during adulthood, the present study systematically investigated how MIA induced by polyinosinic:polycytidilic acid (a mimic of viral double stranded RNA) affected microglial immunoreactivity along the migration and maturation trajectories in the brains of male and female rat offspring at postnatal day (PND) 2. The immunohistochemistry revealed significant changes in the density of IBA-1 immunoreactive cells in the corpus callosum, somatosensory cortex, striatum and the sub-regions of the hippocampus of MIA offspring. Male and female MIA offspring displayed markedly altered microglial immunoreactivity in both the tangential and radial migration, as well as maturation, pathways when compared to their sex- and age-matched controls as evidenced by morphology-based cell counting. Given the important roles of microglia in synaptic pruning and neuronal wiring and survival, these changes may lead to structural and functional neurodevelopmental abnormalities, and so contribute to the functional deficits observed in juvenile and adult MIA offspring. Future research is required to systematically determine how MIA affects microglial migration and maturation in rat offspring. This article is protected by copyright. All rights reserved.
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