File(s) under permanent embargo
Late gestation immune activation increases IBA1-positive immunoreactivity levels in the corpus callosum of adult rat offspring
journal contributionposted on 2023-05-19, 18:42 authored by Duchatel, RJ, Crystal MeehanCrystal Meehan, Harms, LR, Michie, PT, Bigland, MJ, Smith, DW, Walker, FR, Jobling, P, Hodgson, DM, Tooney, PA
Animal models of maternal immune activation study the effects of infection, an environmental risk factor for schizophrenia, on brain development. Microglia activation and cytokine upregulation may have key roles in schizophrenia neuropathology. We hypothesised that maternal immune activation induces changes in microglia and cytokines in the brains of the adult offspring. Maternal immune activation was induced by injecting polyriboinosinic:polyribocytidylic acid into pregnant rats on gestational day (GD) 10 or GD19, with brain tissue collected from the offspring at adulthood. We observed no change in Iba1, Gfap, IL1-βand TNF-α mRNA levels in the cingulate cortex (CC) in adult offspring exposed to maternal immune activation. Prenatal exposure to immune activation had a significant main effect on microglial IBA1-positive immunoreactive material (IBA1+IRM) in the corpus callosum; post-hoc analyses identified a significant increase in GD19 offspring, but not GD10. No change in was observed in the CC. In contrast, maternal immune activation had a significant main effect on GFAP +IRM in the CC at GD19 (not GD10); post-hoc analyses only identified a strong trend towards increased GFAP +IRM in the GD19 offspring, with no white matter changes. This suggests late gestation maternal immune activation causes subtle alterations to microglia and astrocytes in the adult offspring.
Publication titlePsychiatry research
Department/SchoolSchool of Psychological Sciences
PublisherElsevier Sci Ireland Ltd
Place of publicationCustomer Relations Manager, Bay 15, Shannon Industrial Estate Co, Clare, Ireland
Rights statementCrown Copyright 2018 Published by Elsevier B.V. All rights reserved.