Abstract
Despite the known health risks of tobacco smoking, many people including pregnant women continue smoking. The effects of developmental nicotine exposure are known, but the underlying mechanisms are not well understood. Drosophila melanogaster is a model organism that can be used for uncovering genetic and molecular mechanisms for drugs of abuse. Here I show that Drosophila can be a model to elucidate the mechanisms for nicotine’s effects on a developing organism. Drosophila reared on nicotine food display developmental and behavioral effects similar to those in mammals including decreased survival and weight, increased developmental time, and decreased sensitivity to acute nicotine and ethanol. The Drosophila nicotinic acetylcholine receptor subunit alpha 7 (Dα7) mediates some of these effects. A novel role for Dα7 on ethanol sedation in Drosophila is also shown. Future research taking advantage of the genetic and molecular tools for Drosophila will allow additional discovery of the mechanisms behind the effects of nicotine during development.
Highlights
Tobacco addiction is a worldwide public health issue, accounting for nearly 6 million deaths a year [1,2]
Reduced survival was due to lethality during the larval stages, as the % of eclosed pupae, which represents the amount of eclosed pupae out of the total number of pupae was not significantly different for flies reared on nicotine food versus flies reared in control food (S1A Fig)
I examined if rearing flies on nicotine affects the time it takes to eclose into an adult
Summary
Tobacco addiction is a worldwide public health issue, accounting for nearly 6 million deaths a year [1,2]. Tobacco addiction is a complex disease with social and biological factors. Nicotine is the chemical in tobacco associated with its addictive effects [6,7,8]. Nicotine activates nicotinic acetylcholine receptors (nAChRs) in the brain. These receptors are normally activated by the endogenous ligand, acetylcholine, and have roles in learning and memory, psychomotor behaviors and reward [9]. Exposure to nicotine during development has the potential of affecting several aspects of normal brain development by activating nAChRs in a non-physiological manner
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