Introduction: Maternal immune activation (mIA) is a risk factor for schizophrenia. It is hypothesised that mIA-induced fetal neuroinflammation alters neurodevelopment and predisposes offspring to neuropathology. Using our validated mIA model, exposing pregnant rats to the viral mimetic poly(I:C), we have shown that adult offspring exhibit cognitive deficits comparable to those in schizophrenia, and have genomic methylation changes enriched for oligodendrocyte genes.Aims: Examine the relationship between mIA and altered oligodendrocyte development and how these correspond to the onset of adult cognitive deficits.Methods: Pregnant Wister rats received 10mg/kg bodyweight (i.p.) poly(I:C) or saline on gestational day (GD) 15. Fetal whole brains were collected 24h post-treatment (GD16) for cytokine quantification (ELISA). Prefrontal cortex (PFC) cell density (immunohistochemistry), DNA methylation (pyrosequencing) and mRNA (qPCR) and protein (Western Blot) expression analysis were performed at GD21 and postnatal days 1, 21, 35 and 100. Results were analysed using general linear mixed modelling.Results: mIA induced elevated proinflammatory cytokines, particularly IL-6, in the GD16 brain, followed by developmental changes in DNA methylation and expression of oligodendrocyte-specific genes involved in myelination (Mag, Mbp) and adhesion (Nfasc, Ank3). Notably, an earlier switch from immature to mature forms of MBP protein expression was detected in mIA-offspring, corresponding to altered Mbp gene exon methylation. Meanwhile, decreased astrocyte and oligodendrocyte progenitor cell (OPC), alongside increased oligodendrocyte densities were observed in adolescent and adult PFC.Conclusion: Results indicate inflammation-induced maturation of oligodendrocytes and premature myelin formation, which would restrict developmental prefrontal plasticity and may therefore underscore the adult PFC-mediated cognitive deficits.