Neurobiology of Disease Loss of VGLUT3 Produces Circadian-Dependent Hyperdopaminergia and Ameliorates Motor Dysfunction and L-Dopa-Mediated Dyskinesias in a Model of Parkinson’s Disease
نویسندگان
چکیده
Christopher B. Divito,1 Kathy Steece-Collier,3 Daniel T. Case,1 Sean-Paul G. Williams,1 Jennifer A. Stancati,3 Lianteng Zhi,4 Maria E. Rubio,2 X Caryl E. Sortwell,3 Timothy J. Collier,3 David Sulzer,5 Robert H. Edwards,6 Hui Zhang,4 and Rebecca P. Seal1,2 1Department of Neurobiology and 2Department of Otolaryngology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15260, 3Michigan State University, College of Human Medicine, Department of Translational Science and Molecular Medicine and The Udall Center of Excellence in Parkinson’s Disease Research, Grand Rapids, Michigan 49503, 4Department of Neuroscience, Jefferson College of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, 5Departments of Neurology, Psychiatry, and Pharmacology, Columbia University, New York, New York 10032, and 6Departments of Neurology and Physiology, University of California, San Francisco School of Medicine, San Francisco, California 94143
منابع مشابه
Loss of VGLUT3 Produces Circadian-Dependent Hyperdopaminergia and Ameliorates Motor Dysfunction and l-Dopa-Mediated Dyskinesias in a Model of Parkinson's Disease.
UNLABELLED The striatum is essential for many aspects of mammalian behavior, including motivation and movement, and is dysfunctional in motor disorders such as Parkinson's disease. The vesicular glutamate transporter 3 (VGLUT3) is expressed by striatal cholinergic interneurons (CINs) and is thus well positioned to regulate dopamine (DA) signaling and locomotor activity, a canonical measure of b...
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