Kurt Svoboda, PhD
Associate Professor
Education
Postdoctoral, Physiology & Biophysics, University of Colorado-UCHSC
Postdoctoral, Pharmacology, University of Colorado-UCHSC
PhD, Neurobiology & Behavior, State University of New York at Stony Brook
BA, EPO Biology / Psychology, University of Colorado at Boulder
Interests and Expertise
Research in my laboratory uses zebrafish as a model system to investigate nicotine toxicity and the developmental biology of nicotinic acetylcholine receptors (nAChRs).
Research Synopsis
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 human health concern. 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, and behavioral tools are used to define the mechanism by which transient exposure to nicotine perturbs normal vertebrate embryonic development. 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. Within the next 2-3 years, we will have solidly established zebrafish as a platform to define not only the developmental and behavioral responses to transient nicotine exposures, but we will also be in a strong position to identify the targets downstream of inappropriate nicotinic receptor activation that drives these permanent changes.