Abstract
BackgroundPregnant women may be exposed to nicotine if they smoke or use tobacco products, nicotine replacement therapy, or via e-cigarettes. Prenatal nicotine exposure has been shown to have deleterious effects on the nervous system in mammals including changes in brain size and in the dopaminergic system. The genetic and molecular mechanisms for these changes are not well understood. A Drosophila melanogaster model for these effects of nicotine exposure could contribute to faster identification of genes and molecular pathways underlying these effects. The purpose of this study was to determine if developmental nicotine exposure affects the nervous system of Drosophila melanogaster, focusing on changes to brain size and the dopaminergic system at two developmental stages.ResultsWe reared flies on control or nicotine food from egg to 3rd instar larvae or from egg to adult and determined effectiveness of the nicotine treatment. We used immunohistochemistry to visualize the whole brain and dopaminergic neurons, using tyrosine hydroxylase as the marker. We measured brain area, tyrosine hydroxylase fluorescence, and counted the number of dopaminergic neurons in brain clusters.We detected an increase in larval brain hemisphere area, a decrease in tyrosine hydroxylase fluorescence in adult central brains, and a decrease in the number of neurons in the PPM3 adult dopaminergic cluster. We tested involvement of Dα7, one of the nicotinic acetylcholine receptor subunits, and found it was involved in eclosion, as previously described, but not involved in brain size.ConclusionsWe conclude that developmental nicotine exposure in Drosophila melanogaster affects brain size and the dopaminergic system. Prenatal nicotine exposure in mammals has also been shown to have effects on brain size and in the dopaminergic system. This study further establishes Drosophila melanogaster as model organism to study the effects of developmental nicotine exposure. The genetic and molecular tools available for Drosophila research will allow elucidation of the mechanisms underlying the effects of nicotine exposure during development.
Highlights
Pregnant women may be exposed to nicotine if they smoke or use tobacco products, nicotine replacement therapy, or via e-cigarettes
We expected that flies with developmental nicotine exposure in our experiments would have a significant decrease in the number of flies that survived to adulthood and exhibit developmental delay compared to flies grown on medium without nicotine
These results suggest that activation of Nicotinic acetylcholine receptor (nAChR) that do not contain Drosophila nicotinic acetylcholine receptor alpha 7 subunit (Dα7) subunits by developmental nicotine play a role in regulating larval brain size
Summary
Pregnant women may be exposed to nicotine if they smoke or use tobacco products, nicotine replacement therapy, or via e-cigarettes. According to the 2013 National Survey of Drug Use and Health, 15.4% of pregnant women reported recent cigarette use in the United States of America and this percent has not significantly decreased over the last decade [3] This is in light of the fact that smoking during pregnancy has been shown to be harmful and have multiple consequences on the offspring, including a decrease in developmental viability and perturbations in the neural architecture of the brain, coupled to abnormal behavioral outcomes later in life [1, 4,5,6,7,8,9,10,11,12]. There is little evidence that e-cigarettes are effective for smoking cessation and it has been shown that e-cigarette exposure during development leads to behavioral changes in rodents [17, 18]
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