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Abstract:
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Neural crest cells are precursors to craniofacial elements in vertebrates. In humans,
multiple defects, including neurological, behavioral and morphological abnormalities have been
characterized in children born to chronic alcohol drinkers. Some of these Fetal Alcohol
Syndrome (FAS) related defects have been observed in other vertebrates exposed to ethanol
during development. The goal of this project is to determine how ethanol exposure affects
development of zebrafish neural crest derivatives. With increasing exposure to ethanol, it was
suspected that zebrafish embryos would have more severe craniofacial abnormalities due to
abnormal neural crest cell migration, differentiation, or cell death. Zebrafish embryos were
exposed to varying concentrations of ethanol from approximately 30% epiboly until 24 hours
post fertilization and development was monitored. Embryos were stained with alcian blue to
observe facial cartilage after six days of development. Cartilage length and interocular distance
were measured. Moderate ethanol exposure resulted in increased interocular distance while
higher ethanol concentrations led to a reduction in this distance. As ethanol dose increased, the
length of cartilage elements decreased. These defects are consistent with some pathologies
associated with FAS and may be due to abnormal crest development. |
