Education and academic career
Steiner received a M.S. degree in Biology from the Swiss Federal Institute of Technology (ETH) in Zürich, Switzerland, under the guidance of the behavioral biologist Prof. Karl Bättig. He earned his doctoral degree (Dr. rer. nat.) in Physiological Psychology from the University of Düsseldorf, Germany (1989), with Prof. Joseph P. Huston. [1] Steiner pursued his postdoctoral work with Dr. Charles Gerfen in the Laboratory of Cell Biology at the National Institute of Mental Health (NIMH) in Bethesda, MD, USA (1990-1995). [2]
He then became a Research Assistant Professor in the Department of Anatomy and Neurobiology at the University of Tennessee, College of Medicine and The Center for Neuroscience in Memphis, TN. [2]
Steiner was recruited to the faculty of the Department of Cellular and Molecular Pharmacology at the Chicago Medical School in 2000 and served as the department chair from 2011-2022. [2] In 2018, Steiner joined the newly founded Stanson Toshok Center for Brain Function and Repair at Rosalind Franklin University until his retirement in 2024. [3]
Steiner is a series editor of Elsevier’s Handbook of Behavioral Neuroscience series. [4]
He is also an editor of the “Handbook of Basal Ganglia Structure and Function”, edition 1 (Vol. 20, 2010) and edition 2 (Vol. 24, 2016). [5]
Research
Steiner’s research centered on the functional organization of the basal ganglia, a forebrain system important for movement control, action selection, motor learning and motivational aspects of behavior. [6]
His research focused on the role of the neurotransmitters dopamine and serotonin in the regulation of basal ganglia – cortical interactions. One of the main objectives of this work was to understand how treatments with dopaminergic drugs (e.g., psychostimulants such as cocaine and methylphenidate (Ritalin)) and serotonergic medications (e.g., SSRI antidepressants) interact to cause changes in gene regulation in neurons of the striatum, the most prominent part of the basal ganglia, and how these molecular alterations affect basal ganglia function and behavior. [7]
Steiner and his team were the first to demonstrate that prototypical SSRI antidepressants such as fluoxetine (Prozac) potentiate addiction-related gene regulation in the striatum induced by psychostimulant medications [8] [9] and enhance the abuse/addiction liability of these psychostimulants in animal models of substance use disorder. [10] [11]
His work also revealed that novel atypical SSRI s can attenuate L-DOPA-induced abnormal gene regulation in the striatum and resulting dyskinesia in an animal model of Parkinson’s disease. [12] [13]
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