David F. Wozniak, PhD
Research Professor of Psychiatry
Director, Animal Behavior Core
Taylor Family Institute for Innovative Psychiatric Research - Faculty
Education and Training
B.A., Psychology, Hobart College, Geneva, NY, 1973
M.A. Experimental Psychology, Connecticut College, New London, CT, 1977
Ph.D. Physiological Psychology, Washington University, St. Louis, MO, 1984
Areas of Research Interests
A longstanding research interest of mine involves studying the role of NMDA glutamate receptors in learning and memory and in the neuropathologic changes and cognitive decline associated with aging and rodent models of Alzheimers disease. A more recent research focus involves the study of behavioral disturbances resulting from exposure to certain drugs of abuse (e.g., ethanol, phencyclidine) during the early neonatal period in rodents when synaptogenesis is ongoing. Specifically, treating rodents during the first postnatal week with certain classes of drugs such as those that block NMDA receptors or excessively activate GABAA receptors triggers widespread apoptotic neurodegeneration throughout the developing brain. Rodents treated with these drugs demonstrate severe behavioral and cognitive deficits, particularly during adolescence, although sometimes considerable recovery of function may occur during adulthood. Such research provides reasonable animal models for studying the fetal alcohol syndrome and other developmental neuropsychiatric disorders.
Other areas of interest have resulted from my directing the research activities of the Animal Behavior Core. Much of this work involves characterizing the behavioral phenotypes of many of the mutant mice developed and used by investigators at Washington University. These efforts often result in the establishment of different mouse models of human diseases, with particular reference to evaluating compromised behavioral functions and possible therapeutic treatments.
Jevtovic-Todorovic V, Hartman R, Izumi Y, Benshoff ND, Dikranian K, Zorumski CF, Olney JW, Wozniak DF. Early exposure to common anesthetic agents causes widespread neurodegeneration in the developing rat brain and persistent learning deficits. Journal of Neuroscience, 2003, 23: 876-882. Full Article ->
Wozniak DF, Hartman RE, Boyle MP, Vogt SK, Brooks AR, Tenkova T, Young C, Olney JW, Muglia LJ. Apoptotic neurodegeneration induced by ethanol in neonatal mice is associated with profound learning/memory deficits in juveniles followed by progressive functional recovery in adults. Neurobiology of Disease, 2004, 17: 403-414. Full Article ->
Wozniak DF, Xiao M, Xu L, Yamada KA, and Ornitz DM. Impaired spatial learning and defective theta burst induced LTP in mice lacking fibroblast growth factor 14. Neurobiology of Disease, 2007, 26: 14-26. Full Article ->
Dougherty JD, Maloney SE, Wozniak DF, Rieger MA, Sonneblick L, Coppola G, Mahieu NG, Zhang J, Cai J, Patti GJ, Abrahams BS, Geshwind DH, Heintz N. The disruption of Celf 6, a gene identified by translational profiling of serotonergic neurons, results in autism-related behaviors. Journal of Neuroscience, 2012, 33: 2732-2753. Full Article ->
Diggs-Andrews KA, Tokuda K, Izumi Y, Zorumski C, Wozniak DF, Gutmann DH. Dopamine deficiency underlies learning deficits in Neurofibromatosis-1 model mice. Annals of Neurology, 2013, 73: 309-315. Full Article ->
Wozniak DF, Diggs-Andrews KA, Conyers S, Yuede CM, Dearborn JT, Brown JA, Tokuda K, Izumi Y, Zorumski CF, Gutmann DH. Motivational disturbances and effects of L-dopa administration in Neurofibromatosis-1 model mice. Public Library of Science One, 2013 8(6): e66024. Full Article ->
Funded Research Projects
DOD (Key Personnel): Improving Cognitive and Behavior Function in Genetically-Engineered Mice.
NIDCD (Key Personnel): Amelioration of Presbycusis by Blocking T-Type Calcium Channels and Antiepileptic Drugs
NINDS(Key Personnel):Pathophysiology and Novel Therapies for Batten's Disease
NICHD(Key Personnel):Washington University Intellectual and Developmental Disabilities Research Center (Director, Core E:Animal Models Core/Behavior Subcore)
NINDS(Key Personnel): Optical Imaging and Functional Connectivity Mapping in Mice.
NINDS (Key Personnel): Mechanisms of Seizure-Induced Dendritic Injury.
NINDS (Key Personnel): Influence of Interhemispheric Connectivity on Recovery of Focal Ischemia.