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    Kensuke Futai PhD

    TitleAssistant Professor
    InstitutionUniversity of Massachusetts Medical School
    DepartmentPsychiatry
    AddressUniversity of Massachusetts Medical School
    303 Belmont Street
    Worcester MA 01605
      Other Positions
      InstitutionUMMS - Graduate School of Biomedical Sciences
      DepartmentInterdisciplinary Graduate Program

      InstitutionUMMS - Graduate School of Biomedical Sciences
      DepartmentNeuroscience

      InstitutionUMMS - Programs, Centers and Institutes
      DepartmentBrudnick Neuropsychiatric Research Institute

        Biography 
        awards and honors
        2012 - 2015Whitehall Foundation
        Overview 
        Narrative
        Kensuke Futai, Ph.D.

        The roles of Inhibitory neurons in neuropsychiatric diseases

        Our research is focused on investigating the relationship between the dysregulation of synaptic function and neuropsychiatric diseases such as schizophrenia and autism spectrum disorders (ASD) by exploring the regulatory mechanism of inhibitory neurons-mediated synaptic transmission. Synapses are a specialized junction of cell-cell contacts that allow for communication between neurons. Synaptic transmission is mediated by neurotransmitters that are released from a presynaptic terminal and act on corresponding receptors on the postsynaptic dendrite. In the mammalian central nervous system, the most excitatory neurons use glutamate as a neurotransmitter while inhibitory neurons use GABA. Neuronal signal processing is mediated by the integration of both excitatory and inhibitory synaptic responses. Therefore, precise regulatory mechanisms must exist to maintain the balance of excitatory and inhibitory synaptic transmission “E/I balance”. It is becoming increasingly clear that neuropsychiatric diseases may arise from the dysregulation of inhibitory neuronal function which leads to a change in the E/I balance. This would suggest that the restoration of inhibitory function can be a possible direction for therapeutic direction.

        How can we restore inhibitory function? To answer this question, we must understand how inhibitory neurons are activated by excitatory inputs and how the disease-related molecules dysregulate synaptic function. Unfortunately, not much is known about these important topics. Most of our knowledge on excitatory transmission for example is based on studies between two synaptically connected excitatory neurons, but our understanding of excitatory synapses on inhibitory neurons is limited.

        The first research aim for my laboratory is the characterization of excitatory synaptic transmission on inhibitory neurons. The second research aim is to investigate the roles of autism-related genes, such as neuroligin, neurexin, and Shank in excitatory and inhibitory synaptic transmission. We will use a multidisciplinary approach, building on our experiences in electrophysiology and molecular biology techniques to study the role of inhibitory neurons and disease-related molecules with respect to the E-I balance in the hippocampus and cortex.



        Rotation Projects

        Rotation Projects

        The Futai laboratory seeks highly motivated graduate students who have interest in the roles of risk genes of neuropsychiatric diseases, such as autism and schizophrenia, on neuronal function.Rotation students will typically work side-by-side with Kenny Futai or Postdoctoral Fellows, and give one laboratory meeting presentation at the conclusion of their rotation project.

        Rotation projects

        1. The roles of the risk genes of neuropsychiatric diseases on neuronal structure and synaptic function
        2. The roles of the scaffold molecules in synapse maturation, synaptic transmission and synaptic plasticity
        3. Characterization of gultamate receptors which express in interneruon


        Post Docs

        Postdoctoral Position Available

        A postdoctoral position is available to study in this laboratory. Contact Kensuke Futai for additional details.



        Bibliographic 
        selected publications
        List All   |   Timeline
        1. Bharadwaj R, Jiang Y, Mao W, Jakovcevski M, Dincer A, Krueger W, Garbett K, Whittle C, Tushir JS, Liu J, Sequeira A, Vawter MP, Gardner PD, Casaccia P, Rasmussen T, Bunney WE, Mirnics K, Futai K, Akbarian S. Conserved chromosome 2q31 conformations are associated with transcriptional regulation of GAD1 GABA synthesis enzyme and altered in prefrontal cortex of subjects with schizophrenia. J Neurosci. 2013 Jul 17; 33(29):11839-51.
          View in: PubMed
        2. Futai K, Doty CD, Baek B, Ryu J, Sheng M. Specific trans-synaptic interaction with inhibitory interneuronal neurexin underlies differential ability of neuroligins to induce functional inhibitory synapses. J Neurosci. 2013 Feb 20; 33(8):3612-23.
          View in: PubMed
        3. Almeida S, Zhang Z, Coppola G, Mao W, Futai K, Karydas A, Geschwind MD, Tartaglia MC, Gao F, Gianni D, Sena-Esteves M, Geschwind DH, Miller BL, Farese RV, Gao FB. Induced Pluripotent Stem Cell Models of Progranulin-Deficient Frontotemporal Dementia Uncover Specific Reversible Neuronal Defects. Cell Rep. 2012 Oct 9.
          View in: PubMed
        4. Hayashi Y, Okamoto K, Bosch M, Futai K. Roles of neuronal activity-induced gene products in hebbian and homeostatic synaptic plasticity, tagging, and capture. Adv Exp Med Biol. 2012; 970:335-54.
          View in: PubMed
        5. Jo J, Son GH, Winters BL, Kim MJ, Whitcomb DJ, Dickinson BA, Lee YB, Futai K, Amici M, Sheng M, Collingridge GL, Cho K. Muscarinic receptors induce LTD of NMDAR EPSCs via a mechanism involving hippocalcin, AP2 and PSD-95. Nat Neurosci. 2010 Oct; 13(10):1216-24.
          View in: PubMed
        6. Hoogenraad CC, Popa I, Futai K, Martinez-Sanchez E, Sanchez-Martinez E, Wulf PS, van Vlijmen T, Dortland BR, Oorschot V, Govers R, Monti M, Heck AJ, Sheng M, Klumperman J, Rehmann H, Jaarsma D, Kapitein LC, van der Sluijs P. Neuron specific Rab4 effector GRASP-1 coordinates membrane specialization and maturation of recycling endosomes. PLoS Biol. 2010 Jan; 8(1):e1000283.
          View in: PubMed
        7. Ryu J, Futai K, Feliu M, Weinberg R, Sheng M. Constitutively active Rap2 transgenic mice display fewer dendritic spines, reduced extracellular signal-regulated kinase signaling, enhanced long-term depression, and impaired spatial learning and fear extinction. J Neurosci. 2008 Aug 13; 28(33):8178-88.
          View in: PubMed
        8. Ochiishi T, Futai K, Okamoto K, Kameyama K, Kosik KS. Regulation of AMPA receptor trafficking by delta-catenin. Mol Cell Neurosci. 2008 Dec; 39(4):499-507.
          View in: PubMed
        9. Hung AY, Futai K, Sala C, Valtschanoff JG, Ryu J, Woodworth MA, Kidd FL, Sung CC, Miyakawa T, Bear MF, Weinberg RJ, Sheng M. Smaller dendritic spines, weaker synaptic transmission, but enhanced spatial learning in mice lacking Shank1. J Neurosci. 2008 Feb 13; 28(7):1697-708.
          View in: PubMed
        10. Kim MJ, Futai K, Jo J, Hayashi Y, Cho K, Sheng M. Synaptic accumulation of PSD-95 and synaptic function regulated by phosphorylation of serine-295 of PSD-95. Neuron. 2007 Nov 8; 56(3):488-502.
          View in: PubMed
        11. Futai K, Kim MJ, Hashikawa T, Scheiffele P, Sheng M, Hayashi Y. Retrograde modulation of presynaptic release probability through signaling mediated by PSD-95-neuroligin. Nat Neurosci. 2007 Feb; 10(2):186-95.
          View in: PubMed
        12. Futai K. [Hellow, PSJ]. Nippon Seirigaku Zasshi. 2005; 67(5):183-4.
          View in: PubMed
        13. Nakagawa T, Futai K, Lashuel HA, Lo I, Okamoto K, Walz T, Hayashi Y, Sheng M. Quaternary structure, protein dynamics, and synaptic function of SAP97 controlled by L27 domain interactions. Neuron. 2004 Oct 28; 44(3):453-67.
          View in: PubMed
        14. Sala C, Futai K, Yamamoto K, Worley PF, Hayashi Y, Sheng M. Inhibition of dendritic spine morphogenesis and synaptic transmission by activity-inducible protein Homer1a. J Neurosci. 2003 Jul 16; 23(15):6327-37.
          View in: PubMed
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