TAKAYAMA Chitoshi

写真a

Title

Professor

Researcher Number(JSPS Kakenhi)

60197217
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Current Affiliation Organization 【 display / non-display 】

  • Duty   University of the Ryukyus   Graduate School of Medicine   Professor  

  • Concurrently   University of the Ryukyus   Faculty of Medicine   Professor  

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University 【 display / non-display 】

  • 　
    -
    1987.03

    Keio University   Faculty of Medicine   Graduated

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Study abroad experiences 【 display / non-display 】

  • 1996.03
    -
    1997.09

    Section of Neurobiology, Yale University School of Medicine  

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Academic degree 【 display / non-display 】

  • Hokkaido University -  Doctor of Medical Scinece

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External Career 【 display / non-display 】

  • 1987.04
    -
    1995.10

    Department of Anatomy, Hokkaido University School of Medicine, Research Assistants  

  • 1995.11
    -
    1999.03

    Department of Anatomy, Hokkaido University School of Medicine, Senir Assistant  

  • 2000.04
    -
    2002.12

    Department of Molecular Neuroanatomy, Hokkaido University School of Medicine, Senir Assistant  

  • 2003.01
    -
    2007.03

    Department of Molecular Neuroanatomy, Hokkaido University School of Medicine, Associate Professor  

  • 2007.04
    -
    2010.03

    University of the Ryukyus, Faculty of Medicine, Medicine, Department of Physiological Sciences,Professor  

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Affiliated academic organizations 【 display / non-display 】

  • 1987.05
    -
    Now
     

    The Japanese Association of Anatomists 

  • 1990.04
    -
    Now
     

    Japan Neuroscience Society 

  • 2004.04
    -
    Now
     

    The Japanese Association of Anatomists    Scientific Councillor

  • 2007.04
    -
    Now
     

    Okinawa Medical Science Research Foundation 

  • 2007.04
    -
    Now
     

    The Japanese Association of Anatomists    Scientific Councillor

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Research Interests 【 display / non-display 】

  • Neuroscience

  • Neuroanatomy

  • Gross Anatomy

  • Histology

  • Embryology

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Research Areas 【 display / non-display 】

  • Life Science / Neuroscience-general

  • Life Science / Anatomy and histopathology of nervous system

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Research Theme 【 display / non-display 】

  • GABA roles in development, plastisity and regeneration

  • Molecular and morphologica analysis in GABAergic Signaling in the Developing Brain

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Thesis 【 display / non-display 】

  • Altered Distribution of Inhibitory Synaptic Terminals in Reeler Cerebellum with Special Reference to Malposition of GABAergic Neurons

    1994.09

    DOI

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Published Papers 【 display / non-display 】

  • Specific Expression of KCC2 in the α Cells of Normal and Type 1 Diabetes Model Mouse Pancreatic Islets.

    Shimizu-Okabe C, Okada S, Okamoto S, Masuzaki H, Takayama C

    Acta histochemica et cytochemica ( 日本組織細胞化学会 )  55 ( 1 ) 47 - 56   2022.02 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

    　View Summary

    <p>Gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter in the mature brain; however, it acts excitatory during development. This difference in action depends on the intra­cellular chloride ion concentration, primarily regulated by potassium chloride co-transporter2 (KCC2). Sufficient KCC2 expression results in its inhibitory action. GABA is also abundant in pancreatic islets, where it acts differentially on the islet cells, and is involved in carbohydrate metabolism. However, the mechanisms underlying the differential action remain unknown. We performed immunohistochemistry for glutamic acid decarboxylase (GAD), a synthetic enzyme for GABA, and KCC2 in normal adult islets. GAD was co-localized with insulin in β cells, whereas KCC2 was expressed in glucagon-positive α cells. These results are in line with previous observations that GABA decreases glucagon release but increases insulin release, and suggest that GABA and insulin may work together in reducing blood glucose levels under hyperglycemia. Next, we examined the streptozotocin-induced type1 diabetes mellitus mouse model. GAD and insulin expression levels were markedly decreased. KCC2 was expressed in glucagon-positive cells, whereas insulin- and somatostatin-positive cells were KCC2-negative. These findings suggest that in diabetes model, reduced GABA release may cause disinhibition of glucagon release, resulting in increased blood sugar levels and the maintenance of hyperglycemic state.</p>

  • Developmental Formation of the GABAergic and Glycinergic Networks in the Mouse Spinal Cord

    Shimizu-Okabe C.

    International Journal of Molecular Sciences ( International Journal of Molecular Sciences )  23 ( 2 )   2022.01 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

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  • Slow progression of sciatic nerve degeneration and regeneration after loose ligation through microglial activation and decreased KCC2 levels in the mouse spinal cord ventral horn.

    Yafuso T, Kosaka Y, Shimizu-Okabe C, Okura N, Kobayashi S, Kim J, Matsuda K, Kinjo D, Okabe A, Takayama C

    Neuroscience research     2021.10 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

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  • Disassembly of the apical junctional complex during the transmigration of Leptospira interrogans across polarized renal proximal tubule epithelial cells.

    Sebastián I, Okura N, Humbel BM, Xu J, Hermawan I, Matsuura C, Hall M, Takayama C, Yamashiro T, Nakamura S, Toma C

    Cellular microbiology ( Cellular Microbiology )  23 ( 9 ) e13343   2021.09 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

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  • Development and persistence of neuropathic pain through microglial activation and KCC2 decreasing after mouse tibial nerve injury.

    Kosaka Y, Yafuso T, Shimizu-Okabe C, Kim J, Kobayashi S, Okura N, Ando H, Okabe A, Takayama C

    Brain research ( Brain Research )  1733   146718   2020.04 [ Peer Review Accepted ]

    Type of publication: Research paper (scientific journal)

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Books 【 display / non-display 】

  • Factors Affecting Neurodevelopment

    Shiori Kobayashi, Chigusa Shimizu-Okabe, Jeongtae Kim, Yoshinori Kosaka, Masanobu Sunagawa, Akihito Okabe, Chitoshi Takayama ( Part: Multiple Authorship ,  Development of the GABAergic network in the mouse spinal cord )

    Academic Press is an imprint of Elsevier  2021

    　View Summary

    Gamma-amino butyric acid (GABA) is one of the predominant inhibitory neurotransmitters in the spinal cord and negatively regulates neuronal activity. In this chapter, we describe the mature GABAergic system in the spinal cord and its developmental process from the viewpoints of GABAergic neurons and terminals, GABA receptors, GABAergic action, and the GABA removal system based on morphological studies. A ventral-to-dorsal developmental direction exists in the localization of GABAergic neurons and terminals, shift of GABAergic action from excitatory to inhibitory, and formation of the GABA removal system. Changes in GABAergic action and maturation of the GABA removal system parallel the formation of GABAergic synapses. In the ventral horn, the number of the GABAergic synapses peaks on the day of birth, and these synapses gradually shift to glycinergic synapses after birth. In the dorsal horn, GABAergic synapses continue to increase in number until postnatal day 21, and some become GABA and glycine coreleasing synapses during postnatal development.

  • GABA in autism and related disorders

    Takayama C ( Part: Single Author ,  GABAergic signaling in the developing cerebellum )

    Elsevier Academic Press  2006.04

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    The chapter reviews the GABAergic system, the system in which neurons produce gamma-aminobutyric acid (GABA) as their output, in the cerebellum and the developmental changes in GABAergic signaling, and discusses the way in which GABA exerts its effect on immature neurons during development. The establishment of GABAergic synapses is crucial for the expression of normal and higher brain functions. The key factors for the formation of functional GABAergic synapses are presented and the mechanisms underlying the formation of GABAergic synapses and networks are discussed. GABAergic input plays important roles in cerebellar functions because GABAergic neurons regulate the neuronal activity of Purkinje cells and granule cells that organize the major stream of neural circuitry in the cerebellar cortex. The neuroanatomical analysis of the cerebellar local circuit suggests that GABAergic neurons play a role in lateral inhibition and negative feedback mechanisms on the Purkinje and granule cells. The elimination of GABAergic input from the Golgi cells in the cerebellar granular layer causes overexcitation of granule cells resulting in severe ataxia during the acute phase. Therefore, GABAergic input plays a role in the regulation of glutamatergic hyperexcitation and could be involved in motor coordination. In addition, neuroimaging and biochemical studies indicate a dysfunction in the GABAergic system in the cerebellum of autistic patients. This result suggests that the GABAergic network in the cerebellum might be involved in not only motor function, but also higher brain functions.

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