Microglial Activation in the Developing Rodent Brain Following Binge-Like Alcohol Exposure During the Third Trimester-Equivalent
Date
2015-05
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University of Delaware
Abstract
Previous studies using rat models have looked at microglial activation
following alcohol exposure in the adolescent and adult brains, or the long-term effects of neonatal alcohol exposure. This current study fills in a gap in the literature by observing the short-term immune response of the brain to neonatal alcohol exposure by measuring microglial cell counts, morphological activation, and inflammatory cytokine expression. Animals were exposed to alcohol on postnatal days (PD) 4-9 to model binge-like exposure during the third trimester equivalent in humans, and effects were observed on PD10. We hypothesized that neonatal alcohol exposure would lead to an increase in microglial proliferation, microglial activation (based on morphological status, or appearance), and inflammatory cytokine release, as these effects have been observed in the adolescent and adult brain following alcohol exposure. The results here were mixed, both supporting this hypothesis and contradicting it. A decrease in microglial cell counts was seen in alcohol-exposed (AE) and sham-intubated (SI) animals, possibly indicating an effect of stress on microglial cell number. No significant change in morphological status was found; however, we did see an increase in the pro-inflammatory cytokine IL-1β and the microglial activation marker, CD11b. These findings are significant as they show specific effects of alcohol on microglia in developing brain and possible stress effects on microglial activation.
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Research Subject Categories::MEDICINE::Morphology, cell biology, pathology::Cell biology::Neuroscience, Pyschology, Brain Science