Michael Bubser, Ph.D.
Research Assistant Professor, Pharmacology
- : firstname.lastname@example.org
- : (615) 322-6347
418 Preston Research Building
2220 Pierce Avenue
Nashville, Tennessee - 37212-6600
- : Michael Bubser, Ph.D. - CV
Michael Bubser obtained his doctoral training in the laboratory of Werner J. Schmidt, Ph.D. at the University of Stuttgart in Germany. His graduate studies focused on the behavioural pharmacology of the dopaminergic innervations of the prefrontal cortex of the rat. He also examined the role of competitive and non-competitive antagonists of the N-methyl-D-aspartate (NMDA) subtype of ionotropic glutamate receptors in animal models of Parkinsonâ€™s disease and schizophrenia as well as their impact on dopamine neurochemistry. During his stay at the Netherlands Institute for Brain Research in Amsterdam (The Netherlands) he was intrigued by the possibilities that functional anatomical techniques could contribute to unraveling the interaction of complex brain circuitry.
During his work with Ariel Y. Deutch in the Departments of Psychiatry at Yale University and Vanderbilt University he continued his functional anatomical studies by examining sites and mechanism(s) of action of typical and atypical antipsychotic drugs (APD) and psychostimulants. In particular he investigated novel sites of APD actions in the diencephalon and demonstrated that there is a correlation between the activation of orexin neurons in the lateral hypothalmus and the liability of certain APDs to cause significant weight gain.
When he joined the Vanderbilt Center for Neuroscience Drug Discovery (VCNDD) in 2009 he started applying his knowledge in functional neuroanatomy and behavioural pharmacology to the study of G-protein-coupled receptors (GPCRs). He currently works on characterizing the therapeutic potential of positive allosteric modulators (PAMs) of the metabotropic glutamate receptor 4 (mGluR4) in animal models of Parkinsonâ€™s disease. A second avenue of his research is the study of in vivo actions of muscarinic cholinergic receptor ligands, in particular M1 and M4 PAMs.
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