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Teratogenic effects of 1.5% EtOH in Cranial Blood Vessel development and Neurogenesis in Zebrafish larvae at 72hpf

Fetal alcohol spectrum disorder, which is observed in children who have been exposed to alcohol in utero, is a leading cause of neurodevelopmental disability. Studies in rodents have shown that prenatal ethanol exposure results in decreased blood flow from the umbilical artery to the fetal brain, compromising neuron formation and angiogenesis in the maturing brain. Ethanol (EtOH) has shown to disrupt coronary artery formation in the embryonic zebrafish, but the effects of ethanol on the developing cerebral blood vessels and neurogenesis in zebrafish larvae remains poorly understood. We exposed zebrafish larvae to 1.5% ethanol at 4 hours post fertilization (hpf) for 24 hours and imaged the brain at 72 hpf. We used Tg(fli1:EGFP) to image cerebral blood vessels and Tg(ETvmat2:GFP) to visualize monoaminergic neurons using confocal microscopy. Morphological data collected at 72hpf depicted significantly higher rates of craniofacial deformities, pericardial edema, and severe axial malformations in 1.5% EtOH‐treated embryos in comparison to control. Our preliminary results suggest that EtOH at 1.5% leads to reduced number of cranial vessels and altered vessel branching, and decreased density of telencephalic and hindbrain neurons. These findings lead to questions regarding molecular and vascular disparities in affected regions of the developing brain.