Annette Fleckenstein

RESEARCH:

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.

Using data from the Utah Population Data Base, Dr. Fleckenstein and colleagues have reported that individuals with attention deficit disorder are more likely to develop basal ganglia disorders, including Parkinson's disease.  Ongoing preclinical studies are investigating mechanisms underlying, and the role of psychostimulants in, this phenomenon.

A variety of techniques are employed in Dr. Fleckenstein's laboratory including radioligand binding, monoamine uptake assays, western blotting, autoradiography, and high-performance liquid chromatography to assess alterations in monoaminergic neuronal function after both non-contingent and contingent drug administration.

Additional ongoing studies in Dr. Fleckenstein's laboratory are investigating the impact of comprehensive dental care on mental health and substance use disorder treatment outcomes.

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