Updated on 2025/04/08

写真a

 
HORIGANE Shin-ichiro
 
Organization
Research Institute of Environmental Medicine Division of Stress Recognition and Response Lecturer
Graduate School
Graduate School of Medicine
Title
Lecturer
Contact information
メールアドレス
External link

Degree 1

  1. 博士(医学) ( 2015.3   東京大学 ) 

Research Interests 6

  1. Neuronal circuit formation

  2. Voltage dependent Ca2+ channels (VDCCs)

  3. Neuronal migration

  4. Neurodevelopmental disorders

  5. Live imagign

  6. Calcium signaling

Research Areas 3

  1. Life Science / Neuroscience-general

  2. Life Science / Pathophysiologic neuroscience

  3. Life Science / Neuroscience-general

Research History 4

  1. Nagoya University   Research Institute of Environmental Medicine   Lecturer

    2020.10

  2. Nagoya University   Research Institute of Environmental Medicine   Assistant Professor

    2016.3 - 2020.9

  3. 名古屋大学   環境医学研究所    研究機関研究員

    2015.9 - 2016.2

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    Country:Japan

  4. 東京大学     大学院医学系研究科 神経生化学分野   特任研究員

    2015.4 - 2015.8

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    Country:Japan

Education 3

  1. The University of Tokyo   Graduate School, Division of Medical Sciences

    2011.4 - 2015.3

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    Country: Japan

  2. The University of Tokyo

    2009.4 - 2011.3

  3. University of Tsukuba   Second Cluster of College

    2005.4 - 2009.3

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    Country: Japan

Professional Memberships 3

  1. The Japanese Society for Neurochemistry

  2. Society for Neuroscience

  3. 日本神経科学会

Committee Memberships 1

  1. Frontiers in Molecular Neuroscience   Editorial Board of Neuroplasticity and Development  

    2022.12   

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    Committee type:Other

 

Papers 15

  1. A hyper-activatable <i>CAMK2A</i> variant associated with intellectual disability causes exaggerated long-term potentiation and learning impairments Open Access

    Pan, M; Liu, PW; Ozawa, Y; Arima-Yoshida, F; Dong, GY; Sawahata, M; Mori, D; Nagase, M; Fujii, H; Ueda, S; Yabuuchi, Y; Liu, XZ; Narita, H; Konno, A; Hirai, H; Ozaki, N; Yamada, K; Kidokoro, H; Bito, H; Mizoguchi, H; Watabe, AM; Horigane, SI; Takemoto-Kimura, S

    TRANSLATIONAL PSYCHIATRY   Vol. 15 ( 1 ) page: 95   2025.3

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/s41398-025-03316-4

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  2. Förster resonance energy transfer-based kinase mutation phenotyping reveals an aberrant facilitation of Ca2+/calmodulin-dependent CaMKIIα activity in de novo mutations related to intellectual disability International journal Open Access

    Hajime Fujii, Hiroyuki Kidokoro, Yayoi Kondo, Masahiro Kawaguchi, Shin-ichiro Horigane, Jun Natsume, Sayaka Takemoto-Kimura, Haruhiko Bito

    Frontiers in Molecular Neuroscience   Vol. 15   page: 970031 - 970031   2022.9

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    Language:English   Publishing type:Research paper (scientific journal)  

    CaMKIIα plays a fundamental role in learning and memory and is a key determinant of synaptic plasticity. Its kinase activity is regulated by the binding of Ca2+/CaM and by autophosphorylation that operates in an activity-dependent manner. Though many mutations in CAMK2A were linked to a variety of neurological disorders, the multiplicity of its functional substrates renders the systematic molecular phenotyping challenging. In this study, we report a new case of CAMK2A P212L, a recurrent mutation, in a patient with an intellectual disability. To quantify the effect of this mutation, we developed a FRET-based kinase phenotyping strategy and measured aberrance in Ca2+/CaM-dependent activation dynamics in vitro and in synaptically connected neurons. CaMKIIα P212L revealed a significantly facilitated Ca2+/CaM-dependent activation in vitro. Consistently, this mutant showed faster activation and more delayed inactivation in neurons. More prolonged kinase activation was also accompanied by a leftward shift in the CaMKIIα input frequency tuning curve. In keeping with this, molecular phenotyping of other reported CAMK2A de novo mutations linked to intellectual disability revealed aberrant facilitation of Ca2+/CaM-dependent activation of CaMKIIα in most cases. Finally, the pharmacological reversal of CAMK2A P212L phenotype in neurons was demonstrated using an FDA-approved NMDA receptor antagonist memantine, providing a basis for targeted therapeutics in CAMK2A-linked intellectual disability. Taken together, FRET-based kinase mutation phenotyping sheds light on the biological impact of CAMK2A mutations and provides a selective, sensitive, quantitative, and scalable strategy for gaining novel insights into the molecular etiology of intellectual disability.

    DOI: 10.3389/fnmol.2022.970031

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  3. A Flp-dependent G-CaMP9a transgenic mouse for neuronal imaging in vivo Open Access

    Masayuki Sakamoto, Masatoshi Inoue, Atsuya Takeuchi, Shigetaka Kobari, Tatsushi Yokoyama, Shin-ichiro Horigane, Sayaka Takemoto-Kimura, Manabu Abe, Kenji Sakimura, Masanobu Kano, Kazuo Kitamura, Hajime Fujii, Haruhiko Bito

    Cell Reports Methods   Vol. 2 ( 2 ) page: 100168 - 100168   2022.2

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Elsevier BV  

    DOI: 10.1016/j.crmeth.2022.100168

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  4. Identification of ultra-rare disruptive variants in voltage-gated calcium channel-encoding genes in Japanese samples of schizophrenia and autism spectrum disorder. International journal Open Access

    Chenyao Wang*, Shin-ichiro Horigane*, Minoru Wakamori*, Shuhei Ueda, Takeshi Kawabata, Hajime Fujii, Itaru Kushima, Hiroki Kimura, Kanako Ishizuka, Yukako Nakamura, Yoshimi Iwayama, Masashi Ikeda, Nakao Iwata, Takashi Okada, Branko Aleksic, Daisuke Mori, Takashi Yoshida, Haruhiko Bito, Takeo Yoshikawa, Sayaka Takemoto-Kimura, Norio Ozaki, (*co-first)

    Translational psychiatry   Vol. 12 ( 1 ) page: 84 - 84   2022.2

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

    Several large-scale whole-exome sequencing studies in patients with schizophrenia (SCZ) and autism spectrum disorder (ASD) have identified rare variants with modest or strong effect size as genetic risk factors. Dysregulation of cellular calcium homeostasis might be involved in SCZ/ASD pathogenesis, and genes encoding L-type voltage-gated calcium channel (VGCC) subunits Cav1.1 (CACNA1S), Cav1.2 (CACNA1C), Cav1.3 (CACNA1D), and T-type VGCC subunit Cav3.3 (CACNA1I) recently were identified as risk loci for psychiatric disorders. We performed a screening study, using the Ion Torrent Personal Genome Machine (PGM), of exon regions of these four candidate genes (CACNA1C, CACNA1D, CACNA1S, CACNA1I) in 370 Japanese patients with SCZ and 192 with ASD. Variant filtering was applied to identify biologically relevant mutations that were not registered in the dbSNP database or that have a minor allele frequency of less than 1% in East-Asian samples from databases; and are potentially disruptive, including nonsense, frameshift, canonical splicing site single nucleotide variants (SNVs), and non-synonymous SNVs predicted as damaging by five different in silico analyses. Each of these filtered mutations were confirmed by Sanger sequencing. If parental samples were available, segregation analysis was employed for measuring the inheritance pattern. Using our filter, we discovered one nonsense SNV (p.C1451* in CACNA1D), one de novo SNV (p.A36V in CACNA1C), one rare short deletion (p.E1675del in CACNA1D), and 14 NSstrict SNVs (non-synonymous SNV predicted as damaging by all of five in silico analyses). Neither p.A36V in CACNA1C nor p.C1451* in CACNA1D were found in 1871 SCZ cases, 380 ASD cases, or 1916 healthy controls in the independent sample set, suggesting that these SNVs might be ultra-rare SNVs in the Japanese population. The neuronal splicing isoform of Cav1.2 with the p.A36V mutation, discovered in the present study, showed reduced Ca2+-dependent inhibition, resulting in excessive Ca2+ entry through the mutant channel. These results suggested that this de novo SNV in CACNA1C might predispose to SCZ by affecting Ca2+ homeostasis. Thus, our analysis successfully identified several ultra-rare and potentially disruptive gene variants, lending partial support to the hypothesis that VGCC-encoding genes may contribute to the risk of SCZ/ASD.

    DOI: 10.1038/s41398-022-01851-y

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  5. Distinctive Regulation of Emotional Behaviors and Fear-Related Gene Expression Responses in Two Extended Amygdala Subnuclei With Similar Molecular Profiles. International journal Open Access

    Shuhei Ueda, Masahito Hosokawa, Koji Arikawa, Kiyofumi Takahashi, Mao Fujiwara, Manami Kakita, Taro Fukada, Hiroaki Koyama, Shin-Ichiro Horigane, Keiichi Itoi, Masaki Kakeyama, Hiroko Matsunaga, Haruko Takeyama, Haruhiko Bito, Sayaka Takemoto-Kimura

    Frontiers in molecular neuroscience   Vol. 14   page: 741895 - 741895   2021.9

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    The central nucleus of the amygdala (CeA) and the lateral division of the bed nucleus of the stria terminalis (BNST) are the two major nuclei of the central extended amygdala that plays essential roles in threat processing, responsible for emotional states such as fear and anxiety. While some studies suggested functional differences between these nuclei, others showed anatomical and neurochemical similarities. Despite their complex subnuclear organization, subnuclei-specific functional impact on behavior and their underlying molecular profiles remain obscure. We here constitutively inhibited neurotransmission of protein kinase C-δ-positive (PKCδ+) neurons-a major cell type of the lateral subdivision of the CeA (CeL) and the oval nucleus of the BNST (BNSTov)-and found striking subnuclei-specific effects on fear- and anxiety-related behaviors, respectively. To obtain molecular clues for this dissociation, we conducted RNA sequencing in subnuclei-targeted micropunch samples. The CeL and the BNSTov displayed similar gene expression profiles at the basal level; however, both displayed differential gene expression when animals were exposed to fear-related stimuli, with a more robust expression change in the CeL. These findings provide novel insights into the molecular makeup and differential engagement of distinct subnuclei of the extended amygdala, critical for regulation of threat processing.

    DOI: 10.3389/fnmol.2021.741895

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  6. Development of an L-type Ca2+ channel-dependent Ca2+ transient during the radial migration of cortical excitatory neurons. International journal Open Access

    Shin-Ichiro Horigane, Shun Hamada, Satoshi Kamijo, Hirokazu Yamada, Miwako Yamasaki, Masahiko Watanabe, Haruhiko Bito, Toshihisa Ohtsuka, Sayaka Takemoto-Kimura

    Neuroscience research   Vol. 169   page: 17 - 26   2021.8

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    Increasing evidence has shown that voltage-gated L-type Ca2+ channels (LTCCs) are crucial for neurodevelopmental events, including neuronal differentiation/migration and neurite morphogenesis/extension. However, the time course of their functional maturation during the development of excitatory neurons remains unknown. Using a combination of fluorescence in situ hybridization and in utero electroporation-based labeling, we found that the transcripts of Cacna1c and Cacna1d, which encode the LTCC pore-forming subunits, were upregulated in the intermediate zone (IZ) during radial migration. Ca2+ imaging using GCaMP6s in acute brain slices showed spontaneous Ca2+ transients in migrating neurons throughout the IZ. Neurons in the IZ upper layer, especially in the multipolar-to-bipolar transition layer (TL), exhibited more frequent Ca2+ transients than adjacent layers and responded to FPL64176, a potent activator of LTCC. Consistently, nimodipine, an LTCC blocker, inhibited spontaneous Ca2+ transients in neurons in the TL. Collectively, we showed a hitherto unknown increased prevalence of LTCC-dependent Ca2+ transients in the TL of the IZ upper layer during the radial migration of excitatory neurons, which could be essential for the regulation of Ca2+-dependent neurodevelopmental processes.

    DOI: 10.1016/j.neures.2020.06.003

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  7. Remote control of neural function by X-ray-induced scintillation. Reviewed International journal

    Takanori Matsubara, Takayuki Yanagida, Noriaki Kawaguchi, Takashi Nakano, Junichiro Yoshimoto, Maiko Sezaki, Hitoshi Takizawa, Satoshi P Tsunoda, Shin-Ichiro Horigane, Shuhei Ueda, Sayaka Takemoto-Kimura, Hideki Kandori, Akihiro Yamanaka, Takayuki Yamashita

    Nature communications   Vol. 12 ( 1 ) page: 4478 - 4478   2021.7

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    Scintillators emit visible luminescence when irradiated with X-rays. Given the unlimited tissue penetration of X-rays, the employment of scintillators could enable remote optogenetic control of neural functions at any depth of the brain. Here we show that a yellow-emitting inorganic scintillator, Ce-doped Gd3(Al,Ga)5O12 (Ce:GAGG), can effectively activate red-shifted excitatory and inhibitory opsins, ChRmine and GtACR1, respectively. Using injectable Ce:GAGG microparticles, we successfully activated and inhibited midbrain dopamine neurons in freely moving mice by X-ray irradiation, producing bidirectional modulation of place preference behavior. Ce:GAGG microparticles are non-cytotoxic and biocompatible, allowing for chronic implantation. Pulsed X-ray irradiation at a clinical dose level is sufficient to elicit behavioral changes without reducing the number of radiosensitive cells in the brain and bone marrow. Thus, scintillator-mediated optogenetics enables minimally invasive, wireless control of cellular functions at any tissue depth in living animals, expanding X-ray applications to functional studies of biology and medicine.

    DOI: 10.1038/s41467-021-24717-1

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  8. A mouse model of Timothy syndrome exhibits altered social competitive dominance and inhibitory neuron development. International journal Open Access

    Shin-Ichiro Horigane, Yukihiro Ozawa, Jun Zhang, Hiroe Todoroki, Pan Miao, Asahi Haijima, Yuchio Yanagawa, Shuhei Ueda, Shigeo Nakamura, Masaki Kakeyama, Sayaka Takemoto-Kimura

    FEBS open bio   Vol. 10 ( 8 ) page: 1436 - 1446   2020.8

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

    Multiple genetic factors related to autism spectrum disorder (ASD) have been identified, but the biological mechanisms remain obscure. Timothy syndrome (TS), associated with syndromic ASD, is caused by a gain-of-function mutation, G406R, in the pore-forming subunit of L-type Ca2+ channels, Cav 1.2. In this study, a mouse model of TS, TS2-neo, was used to enhance behavioral phenotyping and to identify developmental anomalies in inhibitory neurons. Using the IntelliCage, which enables sequential behavioral tasks without human handling and mouse isolation stress, high-social competitive dominance was observed in TS2-neo mice. Furthermore, histological analysis demonstrated inhibitory neuronal abnormalities in the neocortex, including an excess of smaller-sized inhibitory presynaptic terminals in the somatosensory cortex of young adolescent mice and higher numbers of migrating inhibitory neurons from the medial ganglionic eminence during embryonic development. In contrast, no obvious changes in excitatory synaptic terminals were found. These novel neural abnormalities in inhibitory neurons of TS2-neo mice may result in a disturbed excitatory/inhibitory (E/I) balance, a key feature underlying ASD.

    DOI: 10.1002/2211-5463.12924

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  9. Rational Engineering of XCaMPs, a Multicolor GECI Suite for In Vivo Imaging of Complex Brain Circuit Dynamics. Reviewed International journal

    Masatoshi Inoue, Atsuya Takeuchi, Satoshi Manita, Shin-Ichiro Horigane, Masayuki Sakamoto, Ryosuke Kawakami, Kazushi Yamaguchi, Kouhei Otomo, Hiroyuki Yokoyama, Ryang Kim, Tatsushi Yokoyama, Sayaka Takemoto-Kimura, Manabu Abe, Michiko Okamura, Yayoi Kondo, Sean Quirin, Charu Ramakrishnan, Takeshi Imamura, Kenji Sakimura, Tomomi Nemoto, Masanobu Kano, Hajime Fujii, Karl Deisseroth, Kazuo Kitamura, Haruhiko Bito

    Cell   Vol. 177 ( 5 ) page: 1346 - 1360   2019.5

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    To decipher dynamic brain information processing, current genetically encoded calcium indicators (GECIs) are limited in single action potential (AP) detection speed, combinatorial spectral compatibility, and two-photon imaging depth. To address this, here, we rationally engineered a next-generation quadricolor GECI suite, XCaMPs. Single AP detection was achieved within 3-10 ms of spike onset, enabling measurements of fast-spike trains in parvalbumin (PV)-positive interneurons in the barrel cortex in vivo and recording three distinct (two inhibitory and one excitatory) ensembles during pre-motion activity in freely moving mice. In vivo paired recording of pre- and postsynaptic firing revealed spatiotemporal constraints of dendritic inhibition in layer 1 in vivo, between axons of somatostatin (SST)-positive interneurons and apical tufts dendrites of excitatory pyramidal neurons. Finally, non-invasive, subcortical imaging using red XCaMP-R uncovered somatosensation-evoked persistent activity in hippocampal CA1 neurons. Thus, the XCaMPs offer a critical enhancement of solution space in studies of complex neuronal circuit dynamics. VIDEO ABSTRACT.

    DOI: 10.1016/j.cell.2019.04.007

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  10. Calcium signalling: a key regulator of neuronal migration. International journal Open Access

    Horigane SI, Ozawa Y, Yamada H, Takemoto-Kimura S

    Journal of biochemistry   Vol. 165 ( 5 ) page: 401 - 409   2019.5

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    Neuronal migration is a crucial event in neuronal development for the construction of brain architecture and neuronal networks. Newborn neurons proliferate in the germinal zone and start migration toward their final destination. Migrating neurons adopt different routes, cell shapes and migratory modes depending on extracellular factors and outer physical substrates. Intracellular Ca2+ is an essential second messenger that regulates diverse cellular functions by activating Ca2+-dependent signalling molecules that underlie Ca2+-responsive cellular functions. Neuronal migration during brain architecture construction is no exception. Spontaneous Ca2+ transients are observed in several types of migrating neurons, and a series of Ca2+-dependent signalling molecules governing neuronal migration has been identified. In this review, we first summarize the molecular mechanisms that trigger intracellular Ca2+ elevation in migrating neurons. In the latter half of this review, we provide an overview of the literature on Ca2+-dependent signalling molecules underlying neuronal migration.

    DOI: 10.1093/jb/mvz012

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  11. A Critical Neurodevelopmental Role for L-Type Voltage-Gated Calcium Channels in Neurite Extension and Radial Migration. International journal Open Access

    Satoshi Kamijo, Yuichiro Ishii, Shin-Ichiro Horigane, Kanzo Suzuki, Masamichi Ohkura, Junichi Nakai, Hajime Fujii, Sayaka Takemoto-Kimura, Haruhiko Bito

    The Journal of neuroscience : the official journal of the Society for Neuroscience   Vol. 38 ( 24 ) page: 5551 - 5566   2018.6

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    Despite many association studies linking gene polymorphisms and mutations of L-type voltage-gated Ca2+ channels (VGCCs) in neurodevelopmental disorders such as autism and schizophrenia, the roles of specific L-type VGCC during brain development remain unclear. Calcium signaling has been shown to be essential for neurodevelopmental processes such as sculpting of neurites, functional wiring, and fine tuning of growing networks. To investigate this relationship, we performed submembraneous calcium imaging using a membrane-tethered genetically encoded calcium indicator (GECI) Lck-G-CaMP7. We successfully recorded spontaneous regenerative calcium transients (SRCaTs) in developing mouse excitatory cortical neurons prepared from both sexes before synapse formation. SRCaTs originated locally in immature neurites independently of somatic calcium rises and were significantly more elevated in the axons than in dendrites. SRCaTs were not blocked by tetrodoxin, a Na+ channel blocker, but were strongly inhibited by hyperpolarization, suggesting a voltage-dependent source. Pharmacological and genetic manipulations revealed the critical importance of the Cav1.2 (CACNA1C) pore-forming subunit of L-type VGCCs, which were indeed expressed in immature mouse brains. Consistently, knocking out Cav1.2 resulted in significant alterations of neurite outgrowth. Furthermore, expression of a gain-of-function Cav1.2 mutant found in Timothy syndrome, an autosomal dominant multisystem disorder exhibiting syndromic autism, resulted in impaired radial migration of layer 2/3 excitatory neurons, whereas postnatal abrogation of Cav1.2 enhancement could rescue cortical malformation. Together, these lines of evidence suggest a critical role for spontaneous opening of L-type VGCCs in neural development and corticogenesis and indicate that L-type VGCCs might constitute a perinatal therapeutic target for neuropsychiatric calciochannelopathies.SIGNIFICANCE STATEMENT Despite many association studies linking gene polymorphisms and mutations of L-type voltage-gated Ca2+ channels (VGCCs) in neurodevelopmental disorders such as autism and schizophrenia, the roles of specific L-type VGCCs during brain development remain unclear. We here combined the latest Ca2+ indicator technology, quantitative pharmacology, and in utero electroporation and found a hitherto unsuspected role for L-type VGCCs in determining the Ca2+ signaling landscape of mouse immature neurons. We found that malfunctional L-type VGCCs in immature neurons before birth might cause errors in neuritic growth and cortical migration. Interestingly, the retarded corticogenesis phenotype was rescued by postnatal correction of L-type VGCC signal aberration. These findings suggest that L-type VGCCs might constitute a perinatal therapeutic target for neurodevelopment-associated psychiatric disorders.

    DOI: 10.1523/JNEUROSCI.2357-17.2018

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  12. Calmodulin kinases: essential regulators in health and disease Open Access

    Sayaka Takemoto-Kimura, Kanzo Suzuki, Shin-Ichiro Horigane, Satoshi Kamijo, Masatoshi Inoue, Masayuki Sakamoto, Hajime Fujii, Haruhiko Bito

    JOURNAL OF NEUROCHEMISTRY   Vol. 141 ( 6 ) page: 808 - 818   2017.6

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:WILEY  

    Neuronal activity induces intracellular Ca2+ increase, which triggers activation of a series of Ca2+-dependent signaling cascades. Among these, the multifunctional Ca2+/calmodulin-dependent protein kinases (CaMKs, or calmodulin kinases) play key roles in neuronal transmission, synaptic plasticity, circuit development and cognition. The most investigated CaMKs for these roles in neuronal functions are CaMKI, CaMKII, CaMKIV andwe will shed light on these neuronal CaMKs' functions in this review. Catalytically active members of CaMKs currently are CaMKI, CaMKII, CaMKIV and CaMKK. Although they all necessitate the binding of Ca2+ and calmodulin complex (Ca2+/CaM) for releasing autoinhibition, each member of CaMK has distinct activation mechanisms-autophosphorylation mediated autonomy of multimeric CaMKII and CaMKK-dependent phosphoswitch-induced activation of CaMKI or CaMKIV. Furthermore, each CaMK shows distinct subcellular localization that underlies specific compartmentalized function in each activated neuron. In this review, we first summarize these molecular characteristics of each CaMK as to regulation and subcellular localization, and then describe each biological function. In the last section, we also focus on the emerging role of CaMKs in pathophysiological conditions by introducing the recent studies, especially focusing on drug addiction and depression, and discuss how dysfunctional CaMKs may contribute to the pathology of the neuropsychological disorders.

    DOI: 10.1111/jnc.14020

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  13. Exploring the function of calcium-dependent phosphorylation in neuronal morphogenesis and circuit formation. Reviewed International journal

    Takemoto-Kimura S, Horigane S

    Jpn. J. Neuropsychopharmacol   Vol. 37   page: 163 - 167   2017

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  14. Facilitation of axon outgrowth via a Wnt5a-CaMKK-CaMKIα pathway during neuronal polarization Reviewed

    Horigane S, Ageta-Ishihara N, Kamijo S, Fujii H, Okamura M, Kinoshita M, Takemoto-Kimura S, Bito H

    Molecular Brain     2016.1

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    DOI: 10.1186/s13041-016-0189-3

  15. Rational design of a high-affinity, fast, red calcium indicator R-CaMP2 Reviewed

    Inoue M, Takeuchi A, Horigane S, Ohkura M, Gengyo-Ando K, Fujii H, Kamijo S, Takemoto-Kimura S, Kano M, Nakai J, Kitamura K, Bito H

    Nature Methods     2014.11

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    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/nmeth.3185

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MISC 3

  1. Ca2+ imaging in immature cortical neurons Invited

    Shin-ichiro Horigane, Sayaka Takemoto-Kimura

    Cerebral Cortex Development     page: 211 - 219   2024.4

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    DOI: 10.1007/978-1-0716-3810-1

  2. 放射状移動中の大脳皮質興奮性神経細胞におけるL型カルシウムチャネル依存的な一過的細胞内カルシウム濃度上昇の発達

    堀金慎一郎

    神経科学ニュース     2022.2

  3. Intracellular Ca2+ signaling regulates neuronal migration in the developmental period Invited

    HORIGANE Shin-ichiro, Sayaka Takemoto-Kimura

      Vol. 30 ( 1 )   2019.4

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    Publishing type:Article, review, commentary, editorial, etc. (scientific journal)  

Presentations 7

  1. Deciphering a calcium-regulated pathway that controls radial migration of im mature cortical neurons Invited

    HORIGANE Shin-ichiro

    The Joint Congress of the 40th Annual Meeting of Japanese Society of Biological Psychiatry and the 61st Annual Meeting of the Japanese Society for Neurochemistry  2018.9.7 

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  2. Deciphering Ca2+ signaling during radial migration of immature cortical neurons.

    HORIGANE Shin-ichiro

    The 60th Annual Meeting of the Japanese Society for Neurochemistry (JSN)  2017.9.7 

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  3. Deciphering a calcium-regulated pathway that controls radial migration of im mature cortical neurons

    HORIGANE Shin-ichiro

    The 41st Annual Meeting of Japan Neuroscience Society  2018.7.26 

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  4. Deciphering a calcium-regulated pathway that controls radial migration of cortical neurons via the excitation-coupled morphological change

    HORIGANE Shin-ichiro

    Neuro 2019  2019.7.25 

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  5. Calcium transients control a morphogenetic cycle underlying neuronal migratory movement International conference

    HORIGANE Shin-ichiro

    2019.10.23 

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  6. Polarized Ca2+ transients via voltage-gated Ca2+ channels control cyclic nuclear deformation underlying cortical radial migration

    Shin-ichiro Horigane

    2023.9.14 

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  7. Polarized Ca2+ signalling drives neuronal nuclear deformation cycles underlying morphogenetic shape shift during cortical radial migration Invited

    Shin-ichiro Horigane

    2024.5.18 

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Research Project for Joint Research, Competitive Funding, etc. 2

  1. 自閉スペクトラム症の病態理解にむけたカルシウムシグナリング破綻を原因とする神経回路形成障害の解明

    2019.11 - 2021.11

    武田科学振興財団  研究助成 

    堀金慎一郎

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\2000000

  2. 新規病態モデルを用いた多角的解析による発達障害の神経回路病態解明

    2019.9 - 2021.9

    豊秋奨学会  研究費助成 

    堀金慎一郎

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\2500000

KAKENHI (Grants-in-Aid for Scientific Research) 4

  1. カルシウムチャネル異常に起因する自閉スペクトラム症の病態解明と治療開発

    Grant number:24K10490  2024.4 - 2027.3

    科学研究費助成事業  基盤研究(C)

    堀金 慎一郎

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    Authorship:Principal investigator 

    Grant amount:\4550000 ( Direct Cost: \3500000 、 Indirect Cost:\1050000 )

    本研究では、興奮性回路に着目したASD神経回路病態の解明ならびに新たな治療戦略の探索を目的として、3項目の計画を3年間で実施する。
    計画① ASD様行動(社会性障害・繰り返し行動)の評価 【R6年度】
    計画② 興奮性回路の形成障害と神経活動異常の評価 【R6~R7年度】
    計画③ 興奮性神経細胞を標的としたASD治療開発【R7~R8年度】

  2. Deciphering inhibitory neural circuit abnormality underlying autism spectrum disorder and investigation of a new therapeutic approach

    Grant number:22K15638  2022.4 - 2024.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Early-Career Scientists  Grant-in-Aid for Early-Career Scientists

    Shin-ichiro Horigane

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    Authorship:Principal investigator 

    Grant amount:\4550000 ( Direct Cost: \3500000 、 Indirect Cost:\1050000 )

  3. 自閉スペクトラム症に合併する運動機能障害に対する新たな治療戦略の開発

    2022 - 2023

    Shin-ichiro Horigane

  4. Deciphering neural circuit abnormality underlying autism spectrum disorder caused by calcium signaling dysfunction

    Grant number:20K16490  2020.4 - 2022.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Early-Career Scientists

    Shin-ichiro Horigane

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    Authorship:Principal investigator 

    Grant amount:\4160000 ( Direct Cost: \3200000 、 Indirect Cost:\960000 )

    In this project, we aimed to elucidate neural circuit pathology underlying autism spectrum disorder (ASD) and develop a therapeutic method. To address this, 1) we evaluate behavioral abnormality of an ASD-related mouse model expressing mutant L-type Ca2+ channels and found ASD-like behaviors in the mouse model. 2) We also identified dysfunction in neural circuit formation and intracellular Ca2+ dynamics in the mouse model. Furthermore, 3) we developed a brain-wide genetic recombination technique to establish a therapeutic method targeting the mutant L-type Ca2+ channel in this mouse model. These new insights and an experimental method are expected to contribute to developing effective treatment for ASD.

Industrial property rights 2

  1. 細胞内カルシウム動態評価系

    竹本さやか, 堀金慎一郎, 尾崎紀夫, 有岡祐子

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    Date applied:2018.3

    Announcement no:2019-154272  Date announced:2019.9

    Country of applicant:Domestic   Country of acquisition:Domestic

  2. 細胞内カルシウム動態評価系

    竹本さやか, 堀金慎一郎, 尾崎紀夫, 有岡祐子

     More details

    Application no:特願2018-42409 

    Announcement no:特開2019-154272 

 

Teaching Experience (On-campus) 11

  1. 「環境学入門」脳科学と疾患 – 神経回路の形成と疾患

    2024

  2. 基盤医科学実習

    2024

  3. 「環境学入門」脳科学と疾患 – 神経回路の形成と疾患

    2023

  4. 基盤医科学実習

    2023

  5. 基盤医科学実習

    2022

  6. 基盤医学特論「生命現象理解へ向けた多階層アプローチ」

    2022

  7. 基盤医科学実習

    2021

  8. 基盤医科学実習

    2020

  9. 基盤医科学実習

    2019

  10. 基盤医科学実習

    2018

  11. 基盤医科学実習

    2017

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