- Investigator, Unit on Genetics of Cognition and Behavior in the Mood and Anxiety Disorder Program
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.
Academic Articles19
- (2018). Neuropsychiatric Phenotypes Produced by GABA Reduction in Mouse Cortex and Hippocampus. NEUROPSYCHOPHARMACOLOGY. 43(6), 1445-1456.
- (2017). Reduced ethanol drinking following selective cortical interneuron deletion of the GluN2B NMDA receptors subunit. ALCOHOL. 58, 47-51.
- (2015). Cortical GluN2B deletion attenuates punished suppression of food reward-seeking. PSYCHOPHARMACOLOGY. 232(20), 3753-3761.
- (2015). Impaired discrimination learning in interneuronal NMDAR-GluN2B mutant mice. NEUROREPORT. 26(9), 489-494.
- (2014). Brain state-dependent abnormal LFP activity in the auditory cortex of a schizophrenia mouse model. Frontiers in Neuroscience. 8,
- (2014). Dysregulation of the Axonal Trafficking of Nuclear-Encoded Mitochondrial mRNA Alters Neuronal Mitochondrial Activity and Mouse Behavior. Developmental Neurobiology. 74(3), 333-350.
- (2013). Convergence of genetic and environmental factors on parvalbumin-positive interneurons in schizophrenia. Frontiers in Behavioral Neuroscience. 7,
- (2013). GluN2B in corticostriatal circuits governs choice learning and choice shifting. NATURE NEUROSCIENCE. 16(8), 1101-U176.
- (2013). Identification of Transcription Factors for Lineage-Specific ESC Differentiation. Stem Cell Reports. 1(6), 545-559.
- (2013). Social Isolation Exacerbates Schizophrenia-Like Phenotypes via Oxidative Stress in Cortical Interneurons. BIOLOGICAL PSYCHIATRY. 73(10), 1024-1034.
- (2012). Acute D-serine treatment produces antidepressant-like effects in rodents. INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY. 15(8), 1135-1148.
- (2012). GABAergic interneuron origin of schizophrenia pathophysiology. NEUROPHARMACOLOGY. 62(3), 1574-1583.
- (2012). Hilar Mossy Cell Degeneration Causes Transient Dentate Granule Cell Hyperexcitability and Impaired Pattern Separation. NEURON. 76(6), 1189-1200.
- (2010). Loss of GluN2B-Containing NMDA Receptors in CA1 Hippocampus and Cortex Impairs Long-Term Depression, Reduces Dendritic Spine Density, and Disrupts Learning. JOURNAL OF NEUROSCIENCE. 30(13), 4590-4600.
- (2010). Postnatal NMDA receptor ablation in corticolimbic interneurons confers schizophrenia-like phenotypes. NATURE NEUROSCIENCE. 13(1), 76-U240.
- (2010). eIF2 alpha Phosphorylation-Dependent Translation in CA1 Pyramidal Cells Impairs Hippocampal Memory Consolidation without Affecting General Translation. JOURNAL OF NEUROSCIENCE. 30(7), 2582-2594.
- (2009). Lack of kainic acid-induced gamma oscillations predicts subsequent CA1 excitotoxic cell death. EUROPEAN JOURNAL OF NEUROSCIENCE. 30(6), 1036-1055.
- (2006). Inducible and cell-type restricted manipulation in the entorhinal cortex. NEURON. 50(2), 183-185.