Prenatal exposure to
ethanol in humans results in a wide range of developmental abnormalities, including growth deficiency, developmental delay, reduced brain size, permanent neurobehavioral abnormalities and
fetal death. Here we describe the use of Drosophila melanogaster as a model for exploring the effects of
ethanol exposure on development and behavior. We show that developmental
ethanol exposure causes reduced viability, developmental delay and reduced adult body size. We find that flies reared on
ethanol-containing food have smaller brains and imaginal discs, which is due to reduced cell division rather than increased apoptosis. Additionally, we show that, as in mammals, flies reared on
ethanol have altered responses to
ethanol vapor exposure as adults, including increased locomotor activation, resistance to the sedating effects of the
drug and reduced tolerance development upon repeated
ethanol exposure. We have found that the developmental and behavioral defects are largely due to the effects of
ethanol on
insulin signaling; specifically, a reduction in Drosophila
insulin-like
peptide (Dilp) and
insulin receptor expression. Transgenic expression of Dilp
proteins in the larval brain suppressed both the developmental and behavioral abnormalities displayed by
ethanol-reared adult flies. Our results thus establish Drosophila as a useful model system to uncover the complex etiology of
fetal alcohol syndrome.