Nicotine is a drug of abuse, and adverse birth outcomes have been associated with smoking by pregnant women. Since a large number of women continue to smoke or use other nicotine delivery products during pregnancy, developmental exposure to nicotine remains a significant Public Health concern. It is well accepted that exposure of a developing fetus to nicotine from the maternal plasma is linked to a number of abnormalities and has been implicated in significant cognitive, intellectual, and behavioral impairments in offspring. However, the mechanism underlying these outcomes remains unclear. The actions of nicotine are mediated via activation of nicotinic acetylcholine receptors (nAChRs). Although much is known about the repertoire and structure of nAChRs across species, the mechanisms by which nicotine and nAChRs interact to perturb normal vertebrate development is much less well understood. With recent advances in comparative genomics, genetics and toxicology, we are in an outstanding position to fill this critical information gap. In our research, we exploit the advantages of the zebrafish research model where molecular, genetic, physiological, anatomical and behavioral tools are currently being used to define the mechanism (s) by which transient exposure to nicotine perturbs normal vertebrate embryonic development.
The above scenario is framed in a developmental toxicology context. However, it is clear that nicotine is a stimulant which can influence adult human physiology and behaviors such as sleep. We have recently developed a zebrafish platform where we can monitor aspects of sleep behavior in larval zebrafish and determine if nicotine impacts the “sleep-state” of the fish. The goal of this research is to identify mechanism(s) of nicotine-induced sleep disruptions in humans.