20-23 september 2017. Pécs - Hungary
Dopamine D2 Receptor Supersensitivity as a Spectrum of Neurotoxicity and Status in Psychiatric Disorders (Richard M. Kostrzewa)
Dopamine D2 Receptor Supersensitivity as a Spectrum of Neurotoxicity and Status in Psychiatric Disorders (Richard M. Kostrzewa) 2017-09-23 - 13:30-15:30
Venue: Plenary Hall
Alterations in D2 receptor functions are described on several levels and shown to have important roles in behavioral abnormalities relating to human psychiatric disorders.


Richard M. Kostrzewa, Ph.D., Dr.h.c.
Professor, Department of Biomedical Sciences, Quillen College of Medicine
East Tennessee State University


Cynthia Crawford
Department of Psychology, California State University, San Bernadino CA
"Developmental differences in dopamine D2High receptors"

Raul Gainetdinov
Department of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genova, Italy Skolkovo Institute of Science and Technology, Skolkovo, Moscow Region, Russia; Institute of Translational Biomedicine, St. Petersburg State University, St. Petersburg, Russia.
"TAAR1 modulation of D2 receptor sensitivity and dopamine neurotransmission"

Karolina Wydra
Laboratory of Drug Addiction Pharmacology, Institute of Pharmacology Polish Academy of Sciences 
"Allosteric A2A-D2 receptor-receptor interactions in reward behavior"

Richard M. Kostrzewa
Dept Biomedical Sciences, Quillen College of Medicine, East Tennessee State Univ, Johnson City TN, USA.
"Induction of lifelong D2R supersensitivity: relevance to psychiatric disorders"


Abnormality of dopamine D2 receptor (D2R) function, often characterized as D2R supersensitivity (D2RSS), is a commonality of schizopsychiatric disorders in humans. Moreover, virtually all psychotherapeutic agents commonly used for treatment of schizophrenia target, directly or  partially, D2R in brain. The series of topics in this symposium demonstrate an ability to: (1) produce an animal-model of D2RSS - from early ontogeny, mid-stage ontogeny, or late ontogeny; (2) demonstrate signaling processes associated with D2RSS; (3) present functional links between the biologic template of the animal models with overt measurable features of schizophrenia (i.e., BDNF, RGS9, etc.) – neurotoxicological effects in the absence of overt anatomical evidence of neuronal damage; and (4) illustrate the comparable effects of pharmacotherapeutics in modulating biologic and behavioral modalities towards ‘normalcy’ in the animal model versus individuals beset with schizophrenia. A new animal model of schizophrenia, to be presented, has face validity, construct validity and predictive validity with schizophrenia; and imparts several distinct advantages over earlier models, with the impression of being more predictive of pharmacotherapic efficacy.