ArticleMetabolic brain disease2025
The evaluation of maternal immune activation and the development of schizophrenia in offspring of rats.
Article in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Prenatal infection, consequently, maternal immune activation (MIA) contributes to changes in neurogenesis and myelination in fetal development. It may be related to the development of schizophrenia in young adulthood in the offspring. Therefore, this study investigated behavioral and neurochemical parameters in the adult offspring (male and female) of Wistar rats subjected to vaccination against H1N1 and compared these parameters with those of the offspring of rats subjected to Poly(I:C), a moderate immune activation, during pregnancy. Pregnant Wistar rats were divided into three experimental groups: 1) the control group, which received saline; 2) the group administered with influenza A vaccine; 3) the group administered with Poly(I:C). All substances were administered on the ninth day of gestation. At 60 days old, the offspring were submitted to behavioral tests, including olfactory discrimination, open-field, and splash tests. The inflammatory and neurotrophic parameters were evaluated in the frontal cortex, hippocampus, striatum, and olfactory bulb. In general, offspring did not present alterations in the olfactory test, just slight modifications in the open field test. In the splash test, male offspring in the Poly(l:C) and vaccine groups presented anhedonic-like behavior. Both groups also exhibited inflammatory responses and alterations in neurotrophins in response to the Poly(I:C) and vaccine. In conclusion, both Poly(I:C) and H1N1 vaccine showed some behavioral and/or biochemical alteration. However, these changes depend on sex, behavioral and biochemical tests, or brain structure evaluated. More studies are needed to assess different parameters associated with the pathophysiology of schizophrenia, like oxidative stress and neuronal apoptosis.
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