Fetal alcohol spectrum disorder (FASD) describes a wide range of structural deficits and cognitive impairments. FASD impacts up to 5% of children born in the United States each year, making ethanol one of the most common teratogens. Due to limitations and ethical concerns, studies in humans are limited in their ability to study FASD. Animal models have proven critical in identifying and characterizing the mechanisms underlying FASD. In this review, we will focus on the attributes of zebrafish that make it a strong model in which to study ethanol-induced developmental defects. Zebrafish have several attributes that make it an ideal model in which to study FASD. Zebrafish produced large numbers of externally fertilized, translucent embryos. With a high degree of genetic amenability, zebrafish are at the forefront of identifying and characterizing the gene-ethanol interactions that underlie FASD. Work from multiple labs has shown that embryonic ethanol exposures result in defects in craniofacial, cardiac, ocular, and neural development. In addition to structural defects, ethanol-induced cognitive and behavioral impairments have been studied in zebrafish. Building upon these studies, work has identified ethanol-sensitive loci that underlie the developmental defects. However, analyses show there is still much to be learned of these gene-ethanol interactions. The zebrafish is ideally suited to expand our understanding of gene-ethanol interactions and their impact on FASD. Because of the conservation of gene function between zebrafish and humans, these studies will directly translate to studies of candidate genes in human populations and allow for better diagnosis and treatment of FASD.
Keywords: birth defects; environment; fetal alcohol spectrum disorders; gene-ethanol interactions; genetics; zebrafish.
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