Maternal Immune Activation and Postnatal Anoxia Impair Olfactory Discrimination and Increase Oxidative Stress in the Olfactory Bulb of Wistar Rats

Background Maternal immune activation (MIA) during pregnancy is associated with the development of neurodevelopmental diseases and psychiatric disorders. Early perinatal inflammation also increases the vulnerability of newborns to subsequent episodes of oxygen restriction. MIA causes alterations in the hippocampus, cerebral cortex, and olfactory bulb (OB). However, the combined effects of MIA and postnatal oxygen restriction on the OB have not been thoroughly explored. Objective To investigate the effects of lipopolysaccharide (LPS)-induced MIA associated with postnatal oxygen restriction on olfactory behavior and markers of oxidative stress, antioxidant enzyme activity, and cytokine expression in the OB of young rats. Methods A total of 20 male Wistar offspring were used. The experimental model combined LPS-induced MIA (E17-E21) with postnatal anoxia in pups (P0, 20 min exposure to 100% nitrogen). Two experimental groups were formed: Control ( n = 10) and LPS-A ( n = 10). Olfactory behavior (P34), oxidative stress biomarkers, antioxidant enzyme activity, and cytokine expression (PCR) in the OB (P35) were analyzed. Results Animals in the LPS-A group exhibited preserved gross olfactory detection, yet impaired habituation and discrimination of both non-social and social odors. These behavioral changes were accompanied by elevated oxidative stress markers and reduced antioxidant enzyme activity in the OB, while cytokine expression remained unchanged. Conclusion These results suggest that the redox balance may be an important mechanism linking MIA and oxygen restriction to olfactory dysfunction. This supports the idea that perinatal stress can lead to deficits later in life, consistent with the Developmental Origins of Health and Disease (DOHaD) hypothesis.