Transforming the understanding and treatment of mental illness through research
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 Principal Investigators

Kazutoshi Nakazawa, M.D., Ph.D.
Dr. Nakazawa Photo   Dr. Nakazawa is chief of the Unit on Genetics of Cognition and Behavior in the Mood and Anxiety Disorder Program, National Institute of Mental Health, National Institutes of Health. Dr. Nakazawa received his Ph.D. from Keio University School of Medicine in Tokyo, Japan, investigating the elucidation of molecular diversity of glycosyltransferase families. In 1991, he began post-doctoral training in neuroscience at the Laboratory for Neural Networks, Frontier Research Programs (later joined with the Brain Science Institute) in the RIKEN Institute at Wako, Japan. During this time, his research focused on the molecular and cellular mechanisms of cerebellar long-term depression. In 1995 he moved to the Center for Learning and Memory at Massachusetts Institute of Technology (MIT) as a research fellow, and he became a research associate in 2000. While at MIT, Dr. Nakazawa developed cell type-restricted gene manipulation system in hippocampal CA3 by over-expressing Cre recombinase in transgenic mice.
Research Interests

The major thrust of our research is to understand the mechanisms underlying postnatal development of cortical circuitry and its abnormalities that lead to neuropsychiatric disorders. We are particularly interested in the differential roles of cortical and hippocampal GABAergic neurons and excitatory principal neurons in the refinement of cortical circuitry and function.  Our research strategy is to use cell-type specific genetic manipulations to probe the changes in synaptic and circuitry function that may contribute to the emergence of abnormal behaviors.  We use a variety of experimental approaches including mouse genetics, slice physiology, mouse behavioral testing and in vivo physiology in awake behaving mice. We are optimistic that the combination of these approaches will allow us to develop mouse models of psychiatric illnesses such as mood disorders, epilepsy and schizophrenia.  Our ultimate research goal is to understand the neural basis of ‘neuropsychiatric states’ during mouse behavior through in vivo behavioral and physiological monitoring.

Representative Selected Recent Publications:
  • Jiang, Z., Rompala, G.R., Zhang, S., Cowell, R.M., and Nakazawa, K. Social isolation exacerbates schizophrenia-like phenotypes via oxidative stress in cortical interneurons. Biol. Psychiat. 2013 Jan 21. doi:pii: S0006-3223(12)01088-8. 10.1016/j.biopsych.2012.12.004. [Epub ahead of print] (view)
  • Jinde, S., Zsiros, V., Jiang, Z., Nakao, K., Pickel, J., Kohno, K., Belforte, J.E., and Nakazawa, K. Hilar mossy cell degeneration causes transient dentate granule cell hyperexcitability and impaired pattern separation. Neuron 76, 1189-1200, 2012. (view)
  • Nakazawa, K., Zsiros, V., Jiang, Z., Nakao, K., Kolata, S., Zhang, S., and Belforte, J.E. GABAergic interneuron origin of schizophrenia pathophysiology.  Neuropharmacology, 01.022 . 2011. (view)
  • Jiang, Z., Belforte, J.E., Lu, Y., Yabe, Y., Pickel, J., Smith, C.B., Je, H.-S., Lu, B., and Nakazawa, K. eIF2α phosphorylation-dependent translation in CA1 pyramidal cells impairs hippocampal memory consolidation without affecting general protein synthesis. J. Neurosci. 30, 2582-2594, 2010. (view)
  • Belforte, J.E., Zsiros, V., Sklar, E.R., Jiang, Z., Yu, G., Li, Y., Quinlan, E.M., and Nakazawa, K. Postnatal NMDA receptor ablation in corticolimbic interneurons confers schizophrenia-like phenotypes. Nat. Neurosci, 13, 76-83, 2010 (view) (associated with a featured preview article).
Porter Neuroscience Research Center
Building 35, Rm. 1C915
35 Convent Drive, MSC 3710
Bethesda, MD 20892-3710
Phone: 301-451-3499
Email Dr. Nakazawa  
Fax: 301-480-0123
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This page was last updated May 2, 2011.

 The Division of Intramural Research Programs is within the National Institute of Mental Health (NIMH) which is a part of the National Institutes of Health (NIH), a component of the U.S. Department of Health and Human Services.
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