Abstract
Maternal stress during pregnancy is associated with an increased risk of psychopathology in offspring. Resident immune cells of the brain, microglia, may be mediators of prenatal stress and altered neurodevelopment. Here, we demonstrate that neither the exogenous pro-inflammatory cytokine, interleukin-1β (IL-1β), nor the glucocorticoid hormone, corticosterone, recapitulated the full effects of prenatal stress on the morphology of microglial cells in the cortical plate of embryonic mice; IL-1β effects showed greater similarity to prenatal stress effects on microglia. Unexpectedly, oil vehicle alone, which has antioxidant properties, moderated the effects of prenatal stress on microglia. Microglia changes with prenatal stress were also sensitive to the antioxidant, N-acetylcysteine, suggesting redox dysregulation as a mechanism of prenatal stress.
Highlights
Stress experienced by a mother during pregnancy is a risk factor for neuropsychiatric disorders including autism and schizophrenia in offspring [1,2,3,4,5]
IL-1β significantly increased the density of multivacuolated microglia compared to saline, IL1β did not recapitulate the full effect of Prenatally stressed (PS) on multivacuolated microglia (Fig. 1c, solid line)
We found here that corticosterone and IL-1β each had distinct influences on embryonic microglial cells compared to prenatal stress
Summary
Stress experienced by a mother during pregnancy is a risk factor for neuropsychiatric disorders including autism and schizophrenia in offspring [1,2,3,4,5]. Maternal immune activation (MIA) during pregnancy is a risk factor for neuropsychiatric disorders [6,7,8], suggesting that common maternal and offspring neurodevelopmental mechanisms may be involved. The mechanisms by which lasting, neurobiological alterations are induced in the developing fetal brain by maternal physiological changes have yet to be elucidated and are critically important for translational efforts to prevent psychiatric disorders. Models of MIA have highlighted the importance of alterations in immune factors, such as microglia, in fetal neurodevelopment.
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