- ASSISTANT PROFESSOR Psychiatry
- ASSISTANT PROFESSOR Ophthalmology
- ASSISTANT PROFESSOR Neuroscience
- Hirofumi Morishita is an Assistant Professor of Psychiatry, Neuroscience and Ophthalmology at the Mount Sinai School of Medicine. He is also a faculty member of interdisciplinary Child Health & Development Institute, and Friedman Brain Institute. His research focuses on understanding the mechanisms of experience-dependent brain plasticity during developmental critical period. By combining molecular, circuit, and systems level methodologies in mouse visual cortex, his study identified novel molecular “brakes” on adult plasticity, the removal of which led to successfully restore juvenile brain plasticity in adulthood (Morishita et al. Science 2010). He now aims to translate the critical period principle beyond vision toward understanding of neurodevelopmental disorders such as schizophrenia in his own lab at Mount Sinai School of Medicine starting October 2011.
Hirofumi Morishita received his PhD from Osaka University after Psychiatry residency at National Center Hospital of Neurology and Psychiatry in Tokyo and medical school training at Kyushu University (MD). Before joining Mount Sinai, he was a postdoctoral research fellow at Takao Hensch lab, Children’s Hospital Boston, Harvard Medical School. His postdoctoral work led to the preclinical discovery of therapeutic strategies for functional recovery in adulthood.
Visit the Morishita Lab homepage for more details.
2013 - 2015
Basil O'Connor Starter Scholar Research Awards
March of Dimes
2012 - 2015
2012 - 2014
Young Investigator Award
National Alliance for Research on Schizophrenia and Depression (NARSAD)
2012 - 2013
Early Career-Starter Research Grant
Knights Templar Eye Foundation
American College of Neuropsychopharmacology (ACNP)
ResearchHow much of our behavior and its disorders are determined by our genes and by our environment? This nature-nurture debate has continued for centuries by both philosophers and scientists. We now know our behavior reflects neural circuits sculpted by experience during “critical periods” in postnatal life. Such heightened plasticity declines into adulthood, often limiting recovery of function. On the other hand, the adult brain needs stability. Failed stabilization can disrupt circuit computations by allowing modification by undesirable information, which may lead to mental disorders. How does the brain solve this stability-plasticity dilemma? Our lab is interested in the mechanisms that change the brain’s plasticity across development. Such research carries an impact beyond neuroscience, including strategies for recovery from brain injury in adulthood and therapeutic interventions to psychiatric disorders.
Mechanisms regulating developmental cortical plasticity & cognitive function
By combining molecular biology with in vivo electrophysiological technique in mouse visual cortex, we recently identified two molecular mechanisms that close the critical period to limit adult plasticity: 1) novel functional mechanism (anti-nicotinic signaling by lynx1: Morishita et al., Science 2010), and 2) structural mechanism (myelin signaling: unpublished). Our lab will use these molecular brakes as tools to dissect molecular, circuit and systems level pathogenesis of neurodevelopmental disorders including amblyopia (loss of vision) and schizophrenia. We are particularly interested in the development of top-down projection from other cortical areas to visual cortex and its contribution on visual cortex plasticity as well as cognitive development.
Neurodevelopmental function of emerging psychiatric risk genes
Our long term goal is to translate the critical period principle beyond vision toward understanding of neurodevelopmental disorders such as schizophrenia. In collaboration with divisions of neurodevelomental disorders and psychiatric genomics at Mount Sinai School of medicine, our lab aims to provide neurodevelopmental understanding of the emerging risk genes for psychiatric diseases. Our goal is to effectively modulate key neurodevelopmental events during adolescent critical period for preventive and therapeutic purposes.
Michael Demars PhD
Noreen Bukhari MD PhD
Poromendro Burman BS
Morishita H, Miwa JM, Heintz N, Hensch TK. Lynx1, a cholinergic brake, limits plasticity in adult visual cortex. Science (New York, N.Y.) 2010 Nov; 330(6008).
Morishita H, Hensch TK. Critical period revisited: impact on vision. Current opinion in neurobiology 2008 Feb; 18(1).
Morishita H, Yagi T. Protocadherin family: diversity, structure, and function. Current opinion in cell biology 2007 Oct; 19(5).
Morishita H, Umitsu M, Murata Y, Shibata N, Udaka K, Higuchi Y, Akutsu H, Yamaguchi T, Yagi T, Ikegami T. Structure of the cadherin-related neuronal receptor/protocadherin-alpha first extracellular cadherin domain reveals diversity across cadherin families. The Journal of biological chemistry 2006 Nov; 281(44).
Umitsu M, Morishita H, Murata Y, Udaka K, Akutsu H, Yagi T, Ikegami T. 1H, 13C and 15N resonance assignments of the first cadherin domain of Cadherin-related neuronal receptor (CNR)/protocadherin alpha. Journal of biomolecular NMR 2005 Apr; 31(4).
Morishita H, Kawaguchi M, Murata Y, Seiwa C, Hamada S, Asou H, Yagi T. Myelination triggers local loss of axonal CNR/protocadherin alpha family protein expression. The European journal of neuroscience 2004 Dec; 20(11).
Morishita H, Murata Y, Esumi S, Hamada S, Yagi T. CNR/Pcdhalpha family in subplate neurons, and developing cortical connectivity. Neuroreport 2004 Dec; 15(17).
Tada MN, Senzaki K, Tai Y, Morishita H, Tanaka YZ, Murata Y, Ishii Y, Asakawa S, Shimizu N, Sugino H, Yagi T. Genomic organization and transcripts of the zebrafish Protocadherin genes. Gene 2004 Oct; 340(2).
Murata Y, Hamada S, Morishita H, Mutoh T, Yagi T. Interaction with protocadherin-gamma regulates the cell surface expression of protocadherin-alpha. The Journal of biological chemistry 2004 Nov; 279(47).
Morishita H, Makishima T, Kaneko C, Lee YS, Segil N, Takahashi K, Kuraoka A, Nakagawa T, Nabekura J, Nakayama K, Nakayama KI. Deafness due to degeneration of cochlear neurons in caspase-3-deficient mice. Biochemical and biophysical research communications 2001 Jun; 284(1).
Physicians and scientists on the faculty of the Icahn School of Medicine at Mount Sinai often interact with pharmaceutical, device and biotechnology companies to improve patient care, develop new therapies and achieve scientific breakthroughs. In order to promote an ethical and transparent environment for conducting research, providing clinical care and teaching, Mount Sinai requires that salaried faculty inform the School of their relationships with such companies.
Dr. Morishita has not yet completed reporting of Industry relationships.
Mount Sinai's faculty policies relating to faculty collaboration with industry are posted on our website at http://icahn.mssm.edu/about-us/services-and-resources/faculty-resources/handbooks-and-policies/faculty-handbook. Patients may wish to ask their physician about the activities they perform for companies.
Hess Center for Science and Medicine Floor 9 Room 113
1470 Madison Avenue
New York, NY 10029