Abstract
BackgroundFetal Alcohol Spectrum Disorders (FASD) are a collection of disorders resulting from fetal ethanol exposure, which causes a wide range of physical, neurological and behavioral deficits including heightened susceptibility for alcoholism and addictive disorders. While a number of mechanisms have been proposed for how ethanol exposure disrupts brain development, with selective groups of neurons undergoing reduced proliferation, dysfunction and death, the induction of a new neurotransmitter phenotype by ethanol exposure has not yet been reported.Principal FindingsThe effects of embryonic and larval ethanol exposure on brain development were visually monitored using transgenic zebrafish expressing cell-specific green fluorescent protein (GFP) marker genes. Specific subsets of GFP-expressing neurons were highly sensitive to ethanol exposure, but only during defined developmental windows. In the med12 mutant, which affects the Mediator co-activator complex component Med12, exposure to lower concentrations of ethanol was sufficient to reduce GFP expression in transgenic embryos. In transgenic embryos and larva containing GFP driven by an oxytocin-like (oxtl) promoter, ethanol exposure dramatically up-regulated GFP expression in a small group of hindbrain neurons, while having no effect on expression in the neuroendocrine preoptic area.ConclusionsAlcohol exposure during limited embryonic periods impedes the development of specific, identifiable groups of neurons, and the med12 mutation sensitizes these neurons to the deleterious effects of ethanol. In contrast, ethanol exposure induces oxtl expression in the hindbrain, a finding with profound implications for understanding alcoholism and other addictive disorders.
Highlights
Fetal Alcohol Syndrome (FAS) is the most widely recognized consequence of prenatal alcohol exposure and is a leading cause of mental retardation [1]
Alcohol exposure during limited embryonic periods impedes the development of specific, identifiable groups of neurons, and the med12 mutation sensitizes these neurons to the deleterious effects of ethanol
Transgenic Zebrafish Reveal Neuronal Populations that are Sensitive to Ethanol Treatment
Summary
Fetal Alcohol Syndrome (FAS) is the most widely recognized consequence of prenatal alcohol exposure and is a leading cause of mental retardation [1]. Prenatal ethanol exposure results in a continuum of developmental anomalies leading to a spectrum of physical, mental and behavioral deficits, often with lifelong implications. Low levels of fetal alcohol exposure may result in subtle neurodevelopmental consequences that are not necessarily identified as FASD, yet result in susceptibility to a range of neuropsychiatric and behavioral disorders including attention deficit hyperactivity disorder, depression, psychosis, drug addiction and alcoholism [2,4,5,6,7,8,9]. Fetal Alcohol Spectrum Disorders (FASD) are a collection of disorders resulting from fetal ethanol exposure, which causes a wide range of physical, neurological and behavioral deficits including heightened susceptibility for alcoholism and addictive disorders. While a number of mechanisms have been proposed for how ethanol exposure disrupts brain development, with selective groups of neurons undergoing reduced proliferation, dysfunction and death, the induction of a new neurotransmitter phenotype by ethanol exposure has not yet been reported
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