Researcher(s)
- Luzbeth Guzman, Neuroscience, University of Delaware
- Lily Martinez, Neuroscience, University of Delaware
Faculty Mentor(s)
- Jaclyn Schwarz, Neuroscience, University of Delaware
- Elizabeth Wright-Jin, Neuroscience, N/A
Abstract
Hypoxic-ischemic encephalopathy (HIE), a severe form of brain damage due to oxygen deprivation, affects 1.5 per 1000 live births and results in long-term cognitive and motor deficits. The risk of HIE can be increased by disruptions to the maternal immune system due to deregulation, diabetes, hypertension, or infections. Traditional HIE models often overlook maternal immune activation (MIA) despite its significant role in HIE incidence. Our study introduces a non-invasive HIE model that combines late gestation MIA with postnatal hypoxia. In the lab, using a Cryostat, we sliced brains from the neonatal mice models at 30 nnm. The slicing took place for specific brain regions such as the cerebellum, hippocampus, and dorsal striatum from neonatal mice at 24, 48, and 72 hours post-hypoxia. In the future we will focus on immunofluorescence with Iba1 (general microglia maker) and CD68 (microglia phagocytic marker) antibodies to analyze microglial activation and phagocytosis. Additionally, we assessed the social behavior of HIE models using a three-chamber sociability test to understand the impact of hypoxia on social learning and preference. Our findings highlight no statistically significant results in the preference for novel or familiar stimuli. The heterogeneity of HIE outcomes suggest that our two-hit model of MIA and hypoxia offers a more nuanced understanding of HIE in humans. This model may identify novel therapeutic targets for neonates affected by HIE. The study underscores the importance of addressing maternal health disparities to reduce the incidence and severity of neonatal hypoxia and related conditions.