Professor and Director of Foundational Sciences, School of Dentistry
Deputy Director, Utah Addiction Center
Neurobiology of Disease
Brain and Behavior
B.S. 1988, Western Michigan University; M.S. 1990, Western Michigan University; Ph.D. 1994, Michigan State University; Postdoctoral Fellow 1994-1995, National Institutes of Health - National Institute on Drug Abuse, Addiction Research Center
Neuropharmacology, neurochemistry and aminergic transporters
Some psychostimulants of abuse can cause persistent damage to dopaminergic and/or serotonergic neurons in rodents, non-human primates and humans. For example, methamphetamine administration causes persistent dopaminergic deficits that, in part, resemble deficits occurring in Parkinson's disease. Dr. Fleckenstein's laboratory investigates receptor-mediated and subcellular mechanisms contributing to these deficits. A particular focus of the laboratory involves investigating the effects of stimulants on monoaminergic transporters, both because of relevance to the neurotoxicity of stimulants, and because of the laboratory's ongoing interest in the abuse liability of these agents.
A variety of techniques are employed in Dr. Fleckenstein's laboratory including radioligand-binding, rotating disk electrode voltammetry, monoamine uptake assays, western blotting, and high performance liquid chromatography to assess alterations in monoaminergic neuronal function after both non-contingent, and more recently, contingent drug administration.
Several research projects are ongoing in Dr. Fleckenstein's laboratory. One involves investigating mechanisms underlying the neurotoxic effects of methamphetamine, with a particular emphasis on the role of aging (e.g., the impact of the transition from adolescence to young adulthood) in this process. Another project involves investigating mechanisms underlying, and the functional consequences of, stimulant-induced vesicular trafficking. A third project involves assessing the identity and functional relevance of high molecular weight plasmalemmal dopamine transporter complexes that form after methamphetamine treatment. A forth involves investigating the impact of methamphetamine self-administration on both acute and long-term changes in monoaminergic neuronal function.