Updated on 2023/06/02

写真a

 
KIYAMA Yuji
 
Organization
Research Field in Medicine and Health Sciences, Medical and Dental Sciences Area Graduate School of Medical and Dental Sciences Advanced Therapeutics Course Functional Biology and Pharmacology Assistant Professor
Title
Assistant Professor

Degree

  • 博士(医学) ( 2001.3   東京大学 )

Research Interests

  • 表現型解析

  • 行動解析

  • 脳プロ

  • 扁桃体

  • 情動

  • 包括脳ネットワーク

  • てんかん

Research Areas

  • Life Science / Neuroscience-general

  • Life Science / Neuroscience-general

  • Life Science / Laboratory animal science

  • Life Science / Basic brain sciences

  • Life Science / Medical biochemistry

  • Life Science / Laboratory animal science

  • Life Science / Neuroscience-general

  • Life Science / Basic brain sciences

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Education

  • The University of Tokyo

    1997.4 - 2001.3

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    Country: Japan

  • Niigata University

    - 1995.3

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    Country: Japan

Research History

  • Kagoshima University   Research Field in Medicine and Health Sciences, Medical and Dental Sciences Area Graduate School of Medical and Dental Sciences Advanced Therapeutics Course Functional Biology and Pharmacology   Assistant Professor

    2019.3

  • Kagoshima University   Assistant Professor

    2019.3

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    Country:Japan

  • The University of Tokyo   Research Center for Advanced Science and Technology   Assistant Professor

    2017.4 - 2019.2

Professional Memberships

  • 日本生化学会

    2019.4

  • 日本神経科学学会

    1998.5

  • 日本分子生物学会

    1997.7

  • THE JAPAN NEUROSCIENCE SOCIETY

  • THE JAPANESE BIOCHEMICAL SOCIETY

  • THE MOLECULAR BIOLOGY SOCIETY OF JAPAN

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Papers

  • Fumiko Goto, Yuji Kiyama, Itone Ogawa, Hiroyuki Okuno, Taeko Ichise, Hirotake Ichise, Motonobu Anai, Tatsuhiko Kodama, Nobuaki Yoshida, Haruhiko Bito, Toshiya Manabe .  Gastrin-releasing peptide regulates fear learning under stressed conditions via activation of the amygdalostriatal transition area .  Molecular Psychiatry27 ( 3 ) 1694 - 1703   2022.1Reviewed International journal

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    Authorship:Corresponding author   Language:English   Publishing type:Research paper (scientific journal)   Publisher:Springer Science and Business Media LLC  

    The amygdala, a critical brain region responsible for emotional behavior, is crucially involved in the regulation of the effects of stress on emotional behavior. In the mammalian forebrain, gastrin-releasing peptide (GRP), a 27-amino-acid mammalian neuropeptide, which is a homolog of the 14-amino-acid amidated amphibian peptide bombesin, is highly expressed in the amygdala. The levels of GRP are markedly increased in the amygdala after acute stress; therefore, it is known as a stress-activated modulator. To determine the role of GRP in emotional behavior under stress, we conducted some behavioral and biochemical experiments with GRP-knockout (KO) mice. GRP-KO mice exhibited a longer freezing response than wild-type (WT) littermates in both contextual and auditory fear (also known as threat) conditioning tests only when they were subjected to acute restraint stress 20 min before the conditioning. To identify the critical neural circuits associated with the regulation of emotional memory by GRP, we conducted Arc/Arg3.1-reporter mapping in the amygdala with an Arc-Venus reporter transgenic mouse line. In the amygdalostriatal transition area (AST) and the lateral side of the basal nuclei, fear conditioning after restraint stress increased neuronal activity significantly in WT mice, and GRP KO was found to negate this potentiation only in the AST. These results indicate that the GRP-activated neurons in the AST are likely to suppress excessive fear expression through the regulation of downstream circuits related to fear learning following acute stress.

    DOI: 10.1038/s41380-021-01408-3

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    Other Link: https://www.nature.com/articles/s41380-021-01408-3

  • Tetsuo Ohnishi, Yuji Kiyama, Fumiko Arima-Yoshida, Mitsutaka Kadota, Tomoe Ichikawa, Kazuyuki Yamada, Akiko Watanabe, Hisako Ohba, Kaori Tanaka, Akihiro Nakaya, Yasue Horiuchi, Yoshimi Iwayama, Manabu Toyoshima, Itone Ogawa, Chie Shimamoto-Mitsuyama, Motoko Maekawa, Shabeesh Balan, Makoto Arai, Mitsuhiro Miyashita, Kazuya Toriumi, Yayoi Nozaki, Rumi Kurokawa, Kazuhiro Suzuki, Akane Yoshikawa, Tomoko Toyota, Toshihiko Hosoya, Hiroyuki Okuno, Haruhiko Bito, Masanari Itokawa, Shigehiro Kuraku, Toshiya Manabe, Takeo Yoshikawa .  Cooperation of LIM domain-binding 2 (LDB2) with EGR in the pathogenesis of schizophrenia. .  EMBO molecular medicine13 ( 4 ) e12574   2021.4Reviewed International journal

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

    Genomic defects with large effect size can help elucidate unknown pathologic architecture of mental disorders. We previously reported on a patient with schizophrenia and a balanced translocation between chromosomes 4 and 13 and found that the breakpoint within chromosome 4 is located near the LDB2 gene. We show here that Ldb2 knockout (KO) mice displayed multiple deficits relevant to mental disorders. In particular, Ldb2 KO mice exhibited deficits in the fear-conditioning paradigm. Analysis of the amygdala suggested that dysregulation of synaptic activities controlled by the immediate early gene Arc is involved in the phenotypes. We show that LDB2 forms protein complexes with known transcription factors. Consistently, ChIP-seq analyses indicated that LDB2 binds to > 10,000 genomic sites in human neurospheres. We found that many of those sites, including the promoter region of ARC, are occupied by EGR transcription factors. Our previous study showed an association of the EGR family genes with schizophrenia. Collectively, the findings suggest that dysregulation in the gene expression controlled by the LDB2-EGR axis underlies a pathogenesis of subset of mental disorders.

    DOI: 10.15252/emmm.202012574

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  • Kiyama Y, Kikkawa YS, Kinoshita M, Matsumoto Y, Kondo K, Fujimoto C, Iwasaki S, Yamasoba T, Manabe T .  The adhesion molecule cadherin 11 is essential for acquisition of normal hearing ability through middle ear development in the mouse. .  Laboratory investigation; a journal of technical methods and pathology98 ( 11 ) 1364 - 1374   2018.7The adhesion molecule cadherin 11 is essential for acquisition of normal hearing ability through middle ear development in the mouse.Reviewed International journal

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    Cadherin 11 (Cdh11), a member of the cadherin adhesion molecule family, is expressed in various regions of the brain as well as the head and ear. To gain further insights into the roles of Cdh11 in the development of the ear, we performed behavioral tests using Cdh11 knockout (KO) mice. KO mice showed reduced acoustic startle responses and increased thresholds for auditory brainstem responses, indicating moderate hearing loss. The auditory bulla volume and ratio of air-filled to non-air-filled space in the middle ear cavity were reduced in KO mice, potentially causing conductive hearing loss. Furthermore, residual mesenchymal and inflammatory cells were observed in the middle ear cavity of KO mice. Cdh11 was expressed in developing mesenchymal cells just before the start of cavitation, indicating that Cdh11 may be directly involved in middle ear cavitation. Since the auditory bulla is derived from the neural crest, the regulation of neural crest-derived cells by Cdh11 may be responsible for structural development. This mutant mouse may be a promising animal model for elucidating the causes of conductive hearing loss and otitis media.

    DOI: 10.1038/s41374-018-0083-y

    PubMed

  • Nakazawa T, Hashimoto R, Sakoori K, Sugaya Y, Tanimura A, Hashimotodani Y, Ohi K, Yamamori H, Yasuda Y, Umeda-Yano S, Kiyama Y, Konno K, Inoue T, Yokoyama K, Inoue T, Numata S, Ohnuma T, Iwata N, Ozaki N, Hashimoto H, Watanabe M, Manabe T, Yamamoto T, Takeda M, Kano M. .  Emerging roles of ARHGAP33 in intracellular trafficking of TrkB and pathophysiology of neuropsychiatric disorders. .  Nature Communications   2016.2Emerging roles of ARHGAP33 in intracellular trafficking of TrkB and pathophysiology of neuropsychiatric disorders.Reviewed

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  • Taniguchi S, Nakazawa T, Tanimura A, Kiyama Y, Tezuka T, Watabe AM, Katayama N, Yokoyama K, Inoue T, Izumi-Nakaseko H, Kakuta S, Sudo K, Iwakura Y, Umemori H, Inoue T, Murphy NP, Hashimoto K, Kano M, Manabe T, Yamamoto T. .  Involvement of NMDAR2A tyrosine phosphorylation in depression-related behaviour. .  EMBO Journal   2009.12Involvement of NMDAR2A tyrosine phosphorylation in depression-related behaviour.Reviewed

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  • Mohieldin M. M. Youssef, Hiro Taiyo Hamada, Esther Suk King Lai, Yuji Kiyama, Mohamed El-Tabbal, Hiroshi Kiyonari, Kohei Nakano, Bernd Kuhn, Tadashi Yamamoto .  TOB is an effector of the hippocampus-mediated acute stress response .  Translational Psychiatry12 ( 1 ) 302   2022.12

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    Language:Japanese   Publishing type:Research paper (scientific journal)   Publisher:Springer Science and Business Media LLC  

    Abstract

    Stress affects behavior and involves critical dynamic changes at multiple levels ranging from molecular pathways to neural circuits and behavior. Abnormalities at any of these levels lead to decreased stress resilience and pathological behavior. However, temporal modulation of molecular pathways underlying stress response remains poorly understood. Transducer of ErbB2.1, known as TOB, is involved in different physiological functions, including cellular stress and immediate response to stimulation. In this study, we investigated the role of TOB in psychological stress machinery at molecular, neural circuit, and behavioral levels. Interestingly, TOB protein levels increased after mice were exposed to acute stress. At the neural circuit level, functional magnetic resonance imaging (fMRI) suggested that intra-hippocampal and hippocampal-prefrontal connectivity were dysregulated in Tob knockout (Tob-KO) mice. Electrophysiological recordings in hippocampal slices showed increased postsynaptic AMPAR-mediated neurotransmission, accompanied by decreased GABA neurotransmission and subsequently altered Excitatory/Inhibitory balance after Tob deletion. At the behavioral level, Tob-KO mice show abnormal, hippocampus-dependent, contextual fear conditioning and extinction, and depression-like behaviors. On the other hand, increased anxiety observed in Tob-KO mice is hippocampus-independent. At the molecular level, we observed changes in factors involved in stress response like decreased stress-induced LCN2 expression and ERK phosphorylation, as well as increased MKP-1 expression. This study introduces TOB as an important modulator in the hippocampal stress signaling machinery. In summary, we reveal a molecular pathway and neural circuit mechanism by which Tob deletion contributes to expression of pathological stress-related behavior.

    DOI: 10.1038/s41398-022-02078-7

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    Other Link: https://www.nature.com/articles/s41398-022-02078-7

  • Keita Mori, Michinori Koebis, Kazuki Nakao, Shizuka Kobayashi, Yuji Kiyama, Masahiko Watanabe, Toshiya Manabe, Yuichi Iino, Atsu Aiba .  Loss of calsyntenin paralogs disrupts interneuron stability and mouse behavior. .  Molecular brain15 ( 1 ) 23 - 23   2022.3Loss of calsyntenin paralogs disrupts interneuron stability and mouse behavior.Reviewed International journal

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    Calsyntenins (CLSTNs) are important synaptic molecules whose molecular functions are not fully understood. Although mutations in calsyntenin (CLSTN) genes have been associated with psychiatric disorders in humans, their function is still unclear. One of the reasons why the function of CLSTNs in the nervous system has not been clarified is the functional redundancy among the three paralogs. Therefore, to investigate the functions of mammalian CLSTNs, we generated triple knockout (TKO) mice lacking all CLSTN paralogs and examined their behavior. The mutant mice tended to freeze in novel environments and exhibited hypersensitivity to stress. Consistent with this, glucose levels under stress were significantly higher in the mutant mice than in the wild-type controls. In particular, phenotypes such as decreased motivation, which had not been reported in single Clstn KO mice, were newly discovered. The TKO mice generated in this study represent an important mouse model for clarifying the function of CLSTN in the future.

    DOI: 10.1186/s13041-022-00909-8

    PubMed

  • 城山 優治, 大西 哲生, 有馬 史子, 門田 満隆, 尾藤 晴彦, 吉川 武男, 真鍋 俊也, 奥野 浩行 .  Ldb2は扁桃体側核におけるArcの発現を制御することでシナプス機能と恐怖条件づけ学習を制御する(Ldb2 modulates synaptic function and fear learning by regulating Arc expression in the lateral nucleus of the amygdala) .  日本生化学会大会プログラム・講演要旨集94回   [P - 861]   2021.11Ldb2は扁桃体側核におけるArcの発現を制御することでシナプス機能と恐怖条件づけ学習を制御する(Ldb2 modulates synaptic function and fear learning by regulating Arc expression in the lateral nucleus of the amygdala)

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    Language:English   Publisher:(公社)日本生化学会  

  • Naruse Y, Miyajima K, Sugiura R, Muto M, Ogano M, Kurebayashi N, Shiozawa T, Kiyama Y, Nagata E, Odagiri K, Maekawa Y, Mt. FUJI trial investigators .  Comparison of delivery catheter-based and stylet-based right ventricular lead placement at the right ventricular septum under fluoroscopic guidance judged by cardiac CT (Mt. FUJI): a study protocol for the Mt. FUJI randomised controlled trial. .  BMJ open11 ( 5 ) e046782   2021.5Comparison of delivery catheter-based and stylet-based right ventricular lead placement at the right ventricular septum under fluoroscopic guidance judged by cardiac CT (Mt. FUJI): a study protocol for the Mt. FUJI randomised controlled trial.

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    Language:English  

    DOI: 10.1136/bmjopen-2020-046782

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  • Mika Terumitsu-Tsujita, Hiroki Kitaura, Ikuo Miura, Yuji Kiyama, Fumiko Goto, Yoshiko Muraki, Shiho Ominato, Norikazu Hara, Anna Simankova, Norihisa Bizen, Kazuhiro Kashiwagi, Takuhiro Ito, Yasuko Toyoshima, Akiyoshi Kakita, Toshiya Manabe, Shigeharu Wakana, Hirohide Takebayashi, Hironaka Igarashi .  Glial pathology in a novel spontaneous mutant mouse of the Eif2b5 gene: a vanishing white matter disease model. .  Journal of neurochemistry154 ( 1 ) 25 - 40   2020.7Invited Reviewed

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    Vanishing white matter disease (VWM) is an autosomal recessive neurological disorder caused by mutation(s) in any subunit of eukaryotic translation initiation factor 2B (eIF2B), an activator of translation initiation factor eIF2. VWM occurs with mutation of the genes encoding eIF2B subunits (EIF2B1, EIF2B2, EIF2B3, EIF2B4, and EIF2B5). However, little is known regarding the underlying pathogenetic mechanisms or how to treat patients with VWM. Here we describe the identification and detailed analysis of a new spontaneous mutant mouse harboring a point mutation in the Eif2b5 gene (p.Ile98Met). Homozygous Eif2b5I98M mutant mice exhibited a small body, abnormal gait, male and female infertility, epileptic seizures, and a shortened lifespan. Biochemical analyses indicated that the mutant eIF2B protein with the Eif2b5I98M mutation decreased guanine nucleotide exchange activity on eIF2, and the level of the endoplasmic reticulum stress marker activating transcription factor 4 was elevated in the 1-month-old Eif2b5I98M brain. Histological analyses indicated up-regulated glial fibrillary acidic protein immunoreactivity in the astrocytes of the Eif2b5I98M forebrain and translocation of Bergmann glia in the Eif2b5I98M cerebellum, as well as increased mRNA expression of an endoplasmic reticulum stress marker, C/EBP homologous protein. Disruption of myelin and clustering of oligodendrocyte progenitor cells were also indicated in the white matter of the Eif2b5I98M spinal cord at 8 months old. Our data show that Eif2b5I98M mutants are a good model for understanding VWM pathogenesis and therapy development. Cover Image for this issue: doi: 10.1111/jnc.14751.

    DOI: 10.1111/jnc.14887

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  • Wakabayashi C, Numakawa T, Odaka H, Ooshima Y, Kiyama Y, Manabe T, Kunugi H, Iwakura Y. .  IL-1 receptor-antagonist (IL-1Ra) knockout mice show anxiety-like behavior by aging. .  Neuroscience Letters   2015.5IL-1 receptor-antagonist (IL-1Ra) knockout mice show anxiety-like behavior by aging.Reviewed

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  • Hamada S, Ogawa I, Yamasaki M, Kiyama Y, Kassai H, Watabe AM, Nakao K, Aiba A, Watanabe M, Manabe T. .  The glutamate receptor GluN2 subunit regulates synaptic trafficking of AMPA receptors in the neonatal mouse brain. .  European Journal of Neuroscience   2014.10The glutamate receptor GluN2 subunit regulates synaptic trafficking of AMPA receptors in the neonatal mouse brain.Reviewed

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  • Inoue T, Hoshina N, Nakazawa T, Kiyama Y, Kobayashi S, Abe T, Yamamoto T, Manabe T, Yamamoto T. .  LMTK3 deficiency causes pronounced locomotor hyperactivity and impairs endocytic trafficking. .  The Journal of Neuroscience   2014.4LMTK3 deficiency causes pronounced locomotor hyperactivity and impairs endocytic trafficking.Reviewed

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  • Delawary M, Tezuka T, Kiyama Y, Yokoyama K, Wada E, Wada K, Manabe T, Yamamoto T, Nakazawa T. .  NMDAR2B tyrosine phosphorylation is involved in thermal nociception. .  Neuroscience Letters   2012.5NMDAR2B tyrosine phosphorylation is involved in thermal nociception.Reviewed

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  • Wakabayashi C, Kiyama Y, Kunugi H, Manabe T, Iwakura Y. .  Age-dependent regulation of depression-like behaviors through modulation of adrenergic receptor α?A subtype expression revealed by the analysis of interleukin-1 receptor antagonist knockout mice. .  Neuroscience   2011.9Age-dependent regulation of depression-like behaviors through modulation of adrenergic receptor α?A subtype expression revealed by the analysis of interleukin-1 receptor antagonist knockout mice.Reviewed

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  • Delawary M, Tezuka T, Kiyama Y, Yokoyama K, Inoue T, Hattori S, Hashimoto R, Umemori H, Manabe T, Yamamoto T, Nakazawa T. .  NMDAR2B tyrosine phosphorylation regulates anxiety-like behavior and CRF expression in the amygdala. .  Molecular Brain   2010.11NMDAR2B tyrosine phosphorylation regulates anxiety-like behavior and CRF expression in the amygdala.Reviewed

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  • Kina S, Tezuka T, Kusakawa S, Kishimoto Y, Kakizawa S, Hashimoto K, Ohsugi M, Kiyama Y, Horai R, Sudo K, Kakuta S, Iwakura Y, Iino M, Kano M, Manabe T, Yamamoto T. .  Involvement of protein-tyrosine phosphatase PTPMEG in motor learning and cerebellar long-term depression. .  European Journal of Neuroscience   2007.10Involvement of protein-tyrosine phosphatase PTPMEG in motor learning and cerebellar long-term depression.Reviewed

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  • Suto F, Tsuboi M, Kamiya H, Mizuno H, Kiyama Y, Komai S, Shimizu M, Sanbo M, Yagi T, Hiromi Y, Chedotal A, Mitchell KJ, Manabe T, Fujisawa H. .  Interactions between plexin-A2, plexin-A4, and semaphorin 6A control lamina-restricted projection of hippocampal mossy fibers. .  Neuron   2007.2Interactions between plexin-A2, plexin-A4, and semaphorin 6A control lamina-restricted projection of hippocampal mossy fibers.Reviewed

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  • Nakazawa T, Komai S, Watabe AM, Kiyama Y, Fukaya M, Arima-Yoshida F, Horai R, Sudo K, Ebine K, Delawary M, Goto J, Umemori H, Tezuka T, Iwakura Y, Watanabe M, Yamamoto T, Manabe T. .  NR2B tyrosine phosphorylation modulates fear learning as well as amygdaloid synaptic plasticity. .  EMBO Journal   2006.6NR2B tyrosine phosphorylation modulates fear learning as well as amygdaloid synaptic plasticity.Reviewed

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  • Takeuchi T, Kiyama Y, Nakamura K, Tsujita M, Matsuda I, Mori H, Munemoto Y, Kuriyama H, Natsume R, Sakimura K, Mishina M. .  Roles of the glutamate receptor epsilon2 and delta2 subunits in the potentiation and prepulse inhibition of the acoustic startle reflex. .  European Journal of Neuroscience   2001.7Roles of the glutamate receptor epsilon2 and delta2 subunits in the potentiation and prepulse inhibition of the acoustic startle reflex.Reviewed

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  • Nakamura K, Manabe T, Watanabe M, Mamiya T, Ichikawa R, Kiyama Y, Sanbo M, Yagi T, Inoue Y, Nabeshima T, Mori H, Mishina M. .  Enhancement of hippocampal LTP, reference memory and sensorimotor gating in mutant mice lacking a telencephalon-specific cell adhesion molecule. .  European Journal of Neuroscience   2001.1Enhancement of hippocampal LTP, reference memory and sensorimotor gating in mutant mice lacking a telencephalon-specific cell adhesion molecule.Reviewed

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  • Morikawa E, Mori H, Kiyama Y, Mishina M, Asano T, Kirino T. .  Attenuation of focal ischemic brain injury in mice deficient in the epsilon1 (NR2A) subunit of NMDA receptor. .  The Journal of Neuroscience   1998.12Attenuation of focal ischemic brain injury in mice deficient in the epsilon1 (NR2A) subunit of NMDA receptor.Reviewed

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  • Kiyama Y, Manabe T, Sakimura K, Kawakami F, Mori H, Mishina M. .  Increased thresholds for long-term potentiation and contextual learning in mice lacking the NMDA-type glutamate receptor epsilon1 subunit. .  The Journal of Neuroscience   1998.9Increased thresholds for long-term potentiation and contextual learning in mice lacking the NMDA-type glutamate receptor epsilon1 subunit.Reviewed

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  • Morita T, Nitta H, Kiyama Y, Mori H, Mishina M. .  Differential expression of two zebrafish emx homeoprotein mRNAs in the developing brain. .  Neuroscience Letters   1995.9Differential expression of two zebrafish emx homeoprotein mRNAs in the developing brain.Reviewed

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MISC

  • Ldb2 modulates synaptic function and fear learning by regulating Arc expression in the lateral nucleus of the amygdala(和訳中)

    城山 優治, 大西 哲生, 有馬 史子, 門田 満隆, 尾藤 晴彦, 吉川 武男, 真鍋 俊也, 奥野 浩行

    日本生化学会大会プログラム・講演要旨集   94回   [P - 861]   2021.11

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  • マウスにおける全身麻酔下手術による扁桃体の神経活動亢進と記憶障害

    城山 優治, 中原 真由美, 大江 将軍, 坂口 茜, 黒江 那彩, 上村 裕一, 奥野 浩行

    日本生化学会大会プログラム・講演要旨集   93回   [P - 626]   2020.9

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  • 術後認知機能障害に関与する大脳神経回路同定の試み

    中原 真由美, 向原 桂香, 大江 将軍, 城山 優治, 奥野 浩行, 上村 裕一

    日本集中治療医学会雑誌   27 ( Suppl. )   504 - 504   2020.9

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  • てんかん発症に至るまでの海馬歯状回 APE欠損をモデルとして

    城山 優治, 奥野 浩行, 内藤 眞, 尾藤 晴彦, 児玉 龍彦, 真鍋 俊也, 穴井 元暢

    日本生化学会大会プログラム・講演要旨集   92回   [1P - 311]   2019.9

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  • 脳における新たな遺伝子発現制御システム「LDB2-EGR軸」と精神疾患の病態生理における役割

    大西哲生, 城山優治, 有馬(吉田)史子, 門田満隆, 田中かおり, 山田一之, 山田一之, 市川智恵, 新井誠, 中谷明弘, 小川糸音, 渡辺明子, 大羽尚子, 豊島学, 島本(光山)知英, 前川素子, BALAN Shabeesh, 岩山佳美, 野崎弥生, ORNTHANALAI Veravej G., 奥野浩行, 尾藤晴彦, 糸川昌成, 工樂樹洋, 真鍋俊也, 吉川武男

    日本分子生物学会年会プログラム・要旨集(Web)   42nd   2019

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  • 哺乳類におけるカルシンテニンの機能 トリプルノックアウトマウスを用いた解析

    森 啓太, 古戎 道典, 小林 静香, 城山 優治, 真鍋 俊也, 饗場 篤, 飯野 雄一

    生命科学系学会合同年次大会   2017年度   [2P - 1171]   2017.12

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    Language:Japanese   Publisher:生命科学系学会合同年次大会運営事務局  

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Presentations

  • 中原 真由美, 向原 桂香, 大江 将軍, 城山 優治, 奥野 浩行, 上村 裕一   術後認知機能障害に関与する大脳神経回路同定の試み  

    日本集中治療医学会雑誌  2020.9  (一社)日本集中治療医学会

  • 森 啓太, 古戎 道典, 小林 静香, 城山 優治, 真鍋 俊也, 饗場 篤, 飯野 雄一   哺乳類におけるカルシンテニンの機能 トリプルノックアウトマウスを用いた解析  

    生命科学系学会合同年次大会  2017.12  生命科学系学会合同年次大会運営事務局

  • 城山 優治, 中原 真由美, 大江 将軍, 坂口 茜, 黒江 那彩, 上村 裕一, 奥野 浩行   マウスにおける全身麻酔下手術による扁桃体の神経活動亢進と記憶障害  

    日本生化学会大会プログラム・講演要旨集  2020.9  (公社)日本生化学会

  • 城山 優治, 奥野 浩行, 内藤 眞, 尾藤 晴彦, 児玉 龍彦, 真鍋 俊也, 穴井 元暢   てんかん発症に至るまでの海馬歯状回 APE欠損をモデルとして  

    日本生化学会大会プログラム・講演要旨集  2019.9  (公社)日本生化学会

  • 城山 優治, 大西 哲生, 有馬 史子, 門田 満隆, 尾藤 晴彦, 吉川 武男, 真鍋 俊也, 奥野 浩行   Ldb2は扁桃体側核におけるArcの発現を制御することでシナプス機能と恐怖条件づけ学習を制御する(Ldb2 modulates synaptic function and fear learning by regulating Arc expression in the lateral nucleus of the amygdala)  

    日本生化学会大会プログラム・講演要旨集  2021.11  (公社)日本生化学会

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    Language:English  

  • 城山 優治, 後藤 史子, 小川 糸音, 吉田 進昭, 尾藤 晴彦, 真鍋 俊也, 奥野 浩行   Gastrin-releasing peptideは急性ストレス下で、amygdalostriatal transition areaを通じて恐怖学習を調節する  

    日本生化学会大会プログラム・講演要旨集  2022.11  (公社)日本生化学会

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    Language:English  

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Works

  • 学生への相談対応に関する研修会

    日本語

    2019.9

Research Projects

  • ストレス下で心の平穏を保つための脳神経回路

    Grant number:19K07799  2019.4 - 2022.3

    日本学術振興会  科学研究費補助金 基盤研究(C) 

    城山優治

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    Authorship:Principal investigator  Grant type:Competitive

  • 脳部位特異性の極めて高い遺伝子ノックダウンマウスの新規作製法の開発とその応用

    Grant number:21200006  2009.4 - 2012.3

    科学研究費補助金  新学術領域研究(研究課題提案型)

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    Authorship:Principal investigator 

  • 活動神経のプロファイリングを通じた扁桃体機能解析

    Grant number:15K01848  2015.4 - 2019.3

    日本学術振興会  科学研究費補助金 基盤研究(C) 

    城山優治

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    Authorship:Principal investigator  Grant type:Competitive

  • ドミナント・ネガティブ型Creを応用した扁桃体特異的遺伝子KOマウスの作成と解析

    Grant number:23700488  2011.4 - 2014.3

    科学研究費補助金  若手研究(B)

  • 前脳特異的な遺伝子欠損マウスの作成と学習・記憶に関する表現型の解析

    1999.4 - 2001.3

    科学研究費補助金  特別研究員奨励費

 

Teaching Experience

  • 生化学

    2019.4

  • 生化学

    2019.3
    Institution:鹿児島大学医学部

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    Level:Undergraduate (specialized)  Country:Japan