Journal
JOURNAL OF NEUROINFLAMMATION
Volume 15, Issue -, Pages -Publisher
BIOMED CENTRAL LTD
DOI: 10.1186/s12974-018-1079-7
Keywords
Prenatal stress; Embryonic brain; Microglia; Corticosterone; Interleukin-1 beta; Antioxidant
Categories
Funding
- Patterson Trust Award Program in Clinical Research
- NIMH [K08 MH086812]
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [P30ES005605] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [R25MH077823] Funding Source: NIH RePORTER
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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-1 beta (IL-1 beta), 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-1 beta 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.
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