Welcome to Yuzaki Lab
    Yuzaki Lab's (Department of Neurophysiology, Keio University School of Medicine) research theme is to elucidate "how neural activity and environmental changes induce memory and learning,、, 、and how they change the neural network itself ."。For details please Click here.
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We await the participation of motivated indivisuals。We will vigorously nurture young researchers who will lead the future of basic science.。
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It is essential to the NMDA receptor-mediated nerve cells cerebellum LTD(J Physiol)2018.11.2.
Kono M, Kakegawa W, Yoshida K, Yuzaki M. Interneuronal NMDA receptors regulate long-term depression and motor learning in the cerebellum.  J Physiol in press, 2018.
NMDA receptor has been well known to be essential for the expression of LTP and LTD, which is considered as the basis for processes of memory。In the previous study、In the important cerebellum to the motor learning、NMDA receptor had been shown to be required for the expression of LTD and LTP。However, since most NMDA receptors in cerebellar Purkinje cells do not express after maturation、One、NMDA receptors expressed in which cells how to control the LTP / LTD was a long-standing mystery。In this paper、Purkinje cells、Granulosa cells、We were challenged with this problem by deficient NMDA receptor gene in each intervening neurons。After all、NMDA receptors expressed mediated nerve cells it was found to be essential for LTD and cerebellum dependent eye movement learning。It does not participate in the LTP。It is the thesis of Kono's graduate students。

C1qL4 controls fusion of myoblasts through the BAI3(Nature Commun)2018.10.30.
Hamoud N, TRAN, Aimi T, Kakegawa W, Lahaie S, Thibault MP, Pelletier A, Wong GW, Kim IS, A comet, Yuzaki M, Bouvier M, JF side. Spatiotemporal regulation of the GPCR activity of BAI3 by C1qL4 and Stabilin-2 controls myoblast fusion.  Nat Commun 9:4470, 2018.
Muscle fibers are created by the fusion of myoblasts。Fusion of myoblasts happened even during muscle regeneration after damage, not only during development、It has been strictly controlled。We've discovered as a molecule to control the strengthening and pruning of climbing fibers of the cerebellum so far BAI3 is、Although the muscle fibers to be involved in the fusion of myoblasts had been shown so far、The detailed molecular mechanism was not well understood。In this paper、C1qL4 suppresses the BAI3、Stabilin-2 has revealed that temporally and spatially controlled fusion of myoblasts by activating。Synapse formation is C1qL1-BAI3 in the cerebellum、The muscle I think it extremely interesting that the C1qL4-BAI3 to control the muscle formation。As a joint research with Canada's Jean-François Côté laboratory、Conference and Kakegawa, Associate Professor of short-term come the Viviane Tran's a graduate student was indebted to Keio。

Caveolin-1 promotes maturation of neurons during development by controlling the transport of caveolae-independent N- cadherin and L1(IScience)2018.8.21.
Shikanai M, Nishimura YV, Sakurai M, Nabeshima YI, Yuzaki M, Kawauchi T. Caveolin-1 Promotes Early Neuronal Maturation via Caveolae-Independent Trafficking of N-Cadherin and L1.  iScience 28;7:53-67, 2018.
Development process of the dendrites of nerve cells are not fully reproduced in the in vitro。For example, juvenile type of neurites but will be trimmed once in the in vivo、This behavior does not know the mechanism may not be observed in in vitro。In this study by observing neurite development process in in vivo by performing intrauterine electroporation、It was revealed that Caveolin-1 controls the development process of dendrites via endocytosis of N- cadherin and L1。Caveolae has not been involved in this process。It is the job of when the Sendai's has been stayed's with Shikanai to yuzu Saki Research。

New light genetics tool PhotonSABER by a clear causal relationship between exercise and learning LTD(Neuron)2018.08.17.
Wataru Kakegawa, Akira Katoh, Sakae Narumi, Eriko Miura, Junko Motohashi, Akiyo Takahashi, Kazuhisa Kohda, Yugo Fukazawa, **Michisuke Yuzaki, *Shinji Matsuda. Optogenetic Control of Synaptic AMPA Receptor Endocytosis Reveals Roles of LTD in Motor Learning.Neuron. 99:985-998, 2018.*Co-corresponding authors; **Lead Author

Access the recommendation on F1000PrimeActivity-dependent endocytosis of AMPA receptors at postsynaptic sites、which underlies long-term depression (LTD), is thought to mediate certain forms of learning and memory in vivo。However、whether LTD at synaptic levels is causally related to learning and memory at system levels has remained unclear。In this Neuron paper、using a new optogenetic tool, termed PhotonSABER, which could acutely and reversibly inhibit LTD in a light-dependent manner、we show that LTD at parallel fiber-Purkinje cell synapses、is essential for eye movement-based motor learning in vivo。Dr. Kakegawa, Associate Professor at Keio University、and Dr. Matsuda, Associate Professor at the University of Electro-Communications、performed all experiments with great helps from Dr. Kato, Associate Professor (Tokai Univ.), Dr. Fukasawa, Professor (Fukui Univ) and Dr. Kohda, Professor (St. Mali University School of Medicine)。

Localization of endogenous Nuroligin-1 cells and subcellular levels in cerebellar circuit(Cerebellum)2018.07.26.
Kazuya Nozawa, Ayumi Hayashi, Junko Motohashi, Yukari H. Takeo, Keiko Matsuda, Michisuke Yuzaki. Cellular and Subcellular Localization of Endogenous Neuroligin-1 in the Cerebellum.Cerebellum in press, 2018.

For antibodies that can be used for immunohistochemical staining there is no、Neuroligin-1 was not well understood until now how localized in any part of the nerve cell。Nozawa-kun, together with Hayashi-san、Of first-year doctoral Nozawa-kun、By using the inserted mouse HA epitope tag to neuroligin-1 gene、Using anti-HA antibody, Nozawa-kun has clarified cellular and sucellular localization of endogenous Neuroligin-1 in the cerebellum。Mouse production was done by Hayashi researcher。

Improvement of ataxic walking of Cbln1-deficient mice by administration of Cbln1,,ja,(Sci Rep),,en,Yanagihara D.  Improvement of cerebellar,,en,ataxic gait by injecting Cbln1 into the cerebellum of cbln1-null mice,,en(Sci Rep)2018.04.18.
Takeuchi E, Ito-Ishida A, Yuzaki M, Yanagihara D. Improvement of cerebellar
ataxic gait by injecting Cbln1 into the cerebellum of cbln1-null mice. Sci Rep 8:6184, 2018.

Cbln1 significant gait ataxia is seen in the deficient mice。This ataxia walking will improve and direct injection to the Cbln1 protein in the mouse cerebellum after mature。But I did not know well how to improve the heck what the walking parameters。In this paper reveals this point by the analysis of walking kinematics、It has resulted in a basic knowledge of in considering the treatment of gait disturbance caused by cerebellar ataxia。It is Takeuchi's your job at the University of Tokyo Ken Yanagihara。Ishida's Yuzusakiken gave a Cbln1 injection experiments to Cbln1-deficient mice。