Chapter 21 - Behavioral genetics of embryonic ethanol exposure in zebrafish: a model for FASD

Abstract

Despite the reported harmful effects of ethanol on a developing fetus, about 30% of women usually admit to consuming alcohol while pregnant. Prenatal ethanol exposure results in a number of behavioral, cognitive, and morphological deficits, collectively termed fetal alcohol spectrum disorder (FASD). In the most extreme cases, the disease is called fetal alcohol syndrome and is characterized by severe facial dysmorphia and cognitive deficits. The milder forms of FASD are more prevalent and their defining characteristics include behavioral deficits, social problems, cognitive impairment, and increased vulnerability to drug addiction later in life. Unfortunately, the milder forms of FASD often go un- or misdiagnosed despite being more prevalent. Traditionally, rodent animal models, but more recently zebrafish too, have been used to model this disease cluster and to investigate possible underlying biological and genetic mechanisms. The zebrafish provides a number of advantages for studying FASD compared to typical rodent animal models, including their small size, transparent embryos, and external fertilization. An impressive array of forward and reverse genetic techniques has been successfully employed with zebrafish, a feature that also makes this species an appropriate model organism for the analysis of human FASD. The purpose of this review is to summarize current knowledge about and methods employed for the modeling and analysis of FASD in zebrafish. It is the hope that a more thorough understanding of the genetic mechanisms underlying mild forms of FASD will aid the development of proper diagnostic criteria and also that identification of novel therapeutic targets will enable the development of efficacious treatment options.