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Hirofumi Morishita

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    Hirofumi Morishita is an Assistant Professor of Psychiatry, Neuroscience and Ophthalmology at the Icahn School of Medicine at Mount Sinai. He is also a faculty member of interdisciplinary Mindich Child Health & Development Institute, and Friedman Brain Institute. His research focuses on understanding the mechanisms of developmental critical periods for cortical maturation to establish perception and cognition relevant to neurodevelopmental and psychiatric disorders. His laboratory takes an integrated approach, combining molecular, anatomical, imaging, electrophysiological, and behavior methodologies using mouse models.

    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 (Morishita et al. Science 2010).

    Visit the Morishita Lab homepage for more details.


  • 2015 - 2020
    National Eye Institute R01 EY024918
    National Institute of Health

  • 2015 - 2015
    Inaugural Faculty Innovative Collaborations-Idea Prize
    Icahn School of Medicine at Mount Sinai

  • 2014 - 2014
    Pilot Grant
    Mindich Child Health & Development Institute Pilot Grant

  • 2013 - 2015
    Basil O'Connor Starter Scholar Research Awards
    March of Dimes

  • 2012 - 2015
    Research Grant
    Whitehall Foundation

  • 2012 - 2014
    Young Investigator Award
    National Alliance for Research on Schizophrenia and Depression (NARSAD)

  • 2012 -
    Travel Award
    American College of Neuropsychopharmacology (ACNP)

  • 2012 - 2014
    Early Career-Starter Research Grant
    Knights Templar Eye Foundation


How 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? The goal of our lab is to identify the mechanisms of developmental critical periods to establish (1) perception and (2) cognition relevant to neurodevelopmental and psychiatric disorders. We take an integrated approach combining molecular, anatomical, imaging, electrophysiological, and behavior methodologies using mouse models.

Mechanisms Regulating Experience-dependent Perceptual Development

Experience-dependent cortical plasticity is heightened during developmental critical periods but declines into adulthood, posing a major challenge to recovery of function following injury or disease later in life. The major goal of our research is to identify the mechanisms of experience-dependent cortical plasticity using visual system, a premier model of critical period, we take an integrated approach, combining molecular, anatomical, imaging, electrophysiological methodologies all in vivo by further incorporating advanced techniques such as in vivo viral gene transfer, optogenetics, chemogenetics, and two-photon time lapse imaging. We also take translational bioinformatics approach to identify pro-plasticity drugs and anti-plastic perturbations. Our study would have direct implications for Amblyopia, a condition with limited adult-applicable treatment affecting 2–5% of the human population, but also for brain injury repair, sensory recovery, and the treatment of neurodevelopmental disorders with sensory perceptual deficits such as autism. Currently our focus is on two regulatory systems of cortical plasticity: (1) endogenous nicotinic ACh Receptor regulators, and (2) proteolytic system.

(1) Regulation of visual cortex plasticity by endogenous regulators of nicotinic AChRs:
Our previous research identified a protein called Lynx1, an endogenous inhibitor of nicotinic acetylcholine receptor, acts as a brake to limit plasticity in the adult brain. We established that removing Lynx1 reintroduces plasticity and restores normal vision in a mouse model of Amblyopia, which affects 2-4% of the human population, exhibits little recovery in adulthood (Morishita et al Science 2010). Our current research aims to dissect cellular and circuit mechanisms of plasticity regulated by Lynx family members.

(2) Regulation of visual cortex plasticity by proteolytic system:
Proteolytic activity of tissue plasminogen activator (tPA) becomes restricted in the adult brain. Understanding the mechanism for the loss of permissive proteolytic activity is, therefore, a key link for improving function in adult brains. By combining in vivo extracellular recordings, patch-clamp electrophysiology with optogenetics, pharmacogenetics, and cell-type specific gain/loss of gene expression through genetic and viral techniques in vivo, we aim to mechanistically dissect the molecular, cellular, and circuit mechanisms of proleolytic regulation of cortical plasticity.

Mechanisms Regulating Prefrontal Cortex-dependent Cognitive Development

Mechanisms driving critical period circuit development are well described in sensory systems—but poorly characterized for complex cognitive behaviors. Identification of a critical period and underlying mechanisms for cognitive circuits and behavior would eventually improve diagnosis, prevention and treatment of psychiatric disorders. Our study aims to examine to what extent a mechanism critical for regulating the critical period for visual cortex development also modulates maturation of frontal cortex-dependent cognitive functions such as attention and social cognition. We combine in vivo circuit-specific manipulations with a translationally-relevant touchscreen behavioral testing system to identify the developmental regulatory mechanism of cognitive function from the molecular, circuit to the behavioral level. For this line of research, we actively collaborate with division of psychiatric genomics, neurodevelopmental disorders, and psychiatric epigenomics at Mount Sinai.

Laboratory Members:
Mari Sajo PhD: Postdoctoral Fellow
Hiroyuki Koike PhD: Research Scholar
Milo Smith: PhD Student
Masato Sadahiro: PhD Student
Elisa Nabel: MDPhD Student
Lucy Bicks: PhD Student
Poromendro Burman: Associate Researcher
Giulia Taccheri: Master Student


Bukhari N, Burman PN, Hussein A, Demars MP, Sadahiro M, Brady DM, Tsirka SE, Russo SJ, Morishita H. Unmasking Proteolytic Activity for Adult Visual Cortex Plasticity by the Removal of Lynx1. The Journal of neuroscience : the official journal of the Society for Neuroscience 2015 Sep; 35(37).

Koike H, Demars MP, Short JA, Nabel EM, Akbarian S, Baxter MG, Morishita H. Chemogenetic Inactivation of Dorsal Anterior Cingulate Cortex Neurons Disrupts Attentional Behavior in Mouse. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 2015 Jul;.

Morishita H, Kundakovic M, Bicks L, Mitchell A, Akbarian S. Interneuron epigenomes during the critical period of cortical plasticity: Implications for schizophrenia. Neurobiology of learning and memory 2015 Apr;.

Morishita H, Cabungcal JH, Chen Y, Do KQ, Hensch TK. Prolonged Period of Cortical Plasticity upon Redox Dysregulation in Fast-Spiking Interneurons. Biological psychiatry 2015 Jan;.

Demars MP, Morishita H. Cortical parvalbumin and somatostatin GABA neurons express distinct endogenous modulators of nicotinic acetylcholine receptors. Molecular brain 2014 Oct; 7(1).

Nabel EM, Morishita H. Regulating critical period plasticity: insight from the visual system to fear circuitry for therapeutic interventions. Frontiers in psychiatry 2013 Nov; 4.

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).

Cabungcal JH, Steullet P, Morishita H, Kraftsik R, Cuenod M, Hensch TK, Do KQ. Perineuronal nets protect fast-spiking interneurons against oxidative stress. Proceedings of the National Academy of Sciences of the United States of America 2013 May; 110(22).

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).

Industry Relationships

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.

Below are financial relationships with industry reported by Dr. Morishita during 2014 and/or 2015. Please note that this information may differ from information posted on corporate sites due to timing or classification differences.


  • Asubio Pharmaceuticals, Inc.

Mount Sinai's faculty policies relating to faculty collaboration with industry are posted on our website. Patients may wish to ask their physician about the activities they perform for companies.

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