Pat Levitt

Director, Zilkha Neurogenetic Institute
Provost Professor of Neuroscience, Psychiatry & Pharmacy
Chair, Department of Cell and Neurobiology
Keck School of Medicine of USC

Research Topics

  1. Function and Structure Adaptations in Forebrain Development
  2. Development of Reciprocal Neural Circuitry
  3. Neurodevelopmental Mechanisms of Social Behavior
  4. Genetics of Autism Spectrum Disorder
  5. Impact of early experience on brain development
  6. Gene x Environment interactions in brain disorders

Research Overview

Dr Levitt's research focuses on the development of brain architecture that controls learning, emotional and social behavior in children. His clinical genetics and basic research studies have a long term goal of understanding the biological basis of neurodevelopmental and neuropsychiatric disorders, such as autism and schizophrenia, and how genes and the environment together influence typical and atypical development. A major strategy of the laboratory is to use mouse genetics to manipulate gene expression that impacts brain wiring and the development of social and emotional behavior. He currently has research and training grants from the National Institutes of Health (NIH) and the Simons Foundation, and has held numerous grants from NIH, National Science Foundation, National Association for Research on Schizophrenia and Affective Disorders, Joseph and Esther Klingenstein Foundation, March of Dimes Birth Defects Foundation, and other foundations.

Selected Publications

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Levitt, P. and Campbell, D.B. (2009) The genetic and neurobiological compass points toward common signaling dysfunctions in autism spectrum disorders.  J. Clinical Investigation 119:747-754.

Koshibu, K. and Levitt, P. Gene X environment effects: Stress and memory dysfunctions caused by stress and gonadal factor irregularities during puberty in control and TGF-alpha  hypomorphic mice. Neuropsychopharm. 33(3):557-65, 2008.

Bonnin, A., Torii, M., Wang, L., Rakic, P., and Levitt, P. Serotonin modulates the response of embryonic thalamocortical axons to netrin-1.  Nature Neuroscience 10(5):588-597, 2007.

Campbell, D.B., Sutcliffe, J.S., Ebert, P.J., Militerni, R., Bravaccio, C., Trillo, S., Maurizio, E., Schneider, C., Melmed, R., Sacco, R., Persico, A.M., and Levitt, P. A genetic variant that disrupts MET transcription is associated with autism. Proceedings of the National Academy of Sciences 103(45):16834-9, 2006.

Torii, M. and Levitt, P. Dissociation of corticothalamic and thalamocortical axon targeting by an EphA7-mediated mechanism. Neuron 48: 563-575, 2005.

Eagleson, K.L., Bonnin, A. and Levitt, P. Region- and age-specific deficits in gamma-aminobutyric acidergic neuron development in the telencephalon of the uPAR-/- mouse. J. Comp. Neurol. 489: 449-466, 2005.

Campbell, D.B. and Levitt, P. (2008). Future of individualized psychiatric treatment. Pharmacogenomics 9(5), 493-495.  

Judson, M.C., Bergman, M.Y., Campbell, D.B., Eagleson, K.L., Levitt, P. Dynamic gene and protein expression patterns of the autism-associated Met receptor tyrosine kinase in the developing mouse forebrain. J. Comp. Neurol., 513:511-531, 2009

Catania, E.H., Pimenta, A., and Levitt, P. Genetic deletion of Lsamp causes exaggerated behavioral activation in novel environments. Behavioral Brain Research 188(2):380-90, 2008.

Hammock, L. and Levitt, P. (2006). The discipline of neurobehavioral development: the emerging interface of process that builds circuits and skills. Human Development 49:294-309.