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KATAOKA Yosky
Graduate School of Science, Technology and Innovation / Department of Science, Technology and Innovation
Professor

Researcher basic information

■ Committee History
  • 2005, 日本疲労学会, 評議員, 日本疲労学会

Research activity information

■ Award
  • 2007 日本レーザー治療学会研究奨励賞

  • 2005 日本組織細胞化学会若手研究奨励賞

  • 2004 フロンティアレーザー医学賞

  • 1996 井上研究奨励賞

  • Cytochemistry

  • 1st Award for excellent articles in Japan Society of Histochemistry and

  • 13th Inoue Research Award for Young Scientists

■ MISC
  • Y Kataoka, YL Cui, H Yamada, K Utsunomiya, K Niiya, H Yanase, Y Nakamura, A Mitani, K Kataoka, Y Watanabe
    Various kinds of acute pathological events in the central nervous system, such as ischemia, hemorrhage, and trauma, often cause brain edema. The edema may advance for days or weeks while inducing extensive damage in neural function, regardless of the extent of the original damage, and often results in death. Delayed edema is thought to be vasogenic; how ever, the mechanism underlying edema induction remains unknown. We found delayed vascular cell proliferation with a blood-brain barrier breakdown in and around the gerbil CA1 hippocampus, a region known to be involved in delayed apoptotic neuronal death 2-6 days after transient ischemia. Vascular cell proliferation, assessed by SH-thymidine incorporation, was most prominent 4-6 days after ischemia, and extravasation of exogenously applied dye or endogenous serum albumin from blood vessel was observed concomitantly. We propose neovascularization in delayed neuronal death as a cause of brain edema advancing days after neurological events, (C) 2000 Academic Press.
    ACADEMIC PRESS INC, Jul. 2000, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 273(2) (2), 637 - 641, English

  • Yosky Kataoka, Hiroshi Morii, Kazuyuki Imamura, Yilong Cui, Masayuki Kobayashi, Yasuyoshi Watanabe
    Reversible manipulation of local neurotransmission in brain areas, using controlled spatial and temporal resolution, is one of the powerful techniques used to investigate integrative aspects of brain function. We have developed a novel technique for rapidly inactivating local synaptic transmission, from outside the brain, within seconds or minutes via oxidation of target tissue using a photosensitive dye followed by photoirradiation (photo-dynamic tissue oxidation PDTO). PDTO applied through a defined slit, sharply suppressed excitatory synaptic transmission in rat hippocampal slices and also suppressed in vivo hippocampal neurotransmission reversibly. Furthermore, we manipulated the voluntary movement of gerbils in free-field activity by application of PDTO to the striatum. Also, in freely moving kittens, the development of the visual cortex was manipulated by long-lasting application of PDTO to the eye. Thus, PDTO enables external manipulation of in vivo or in vitro neurotransmission in various clearly defined regions on the submillimeter scale. Suppression of neurotransmission occurred only within the photo-oxidized area which can be histochemically visualized.
    2000, European Journal of Neuroscience, 12(12) (12), 4417 - 4423, English

  • Yilong Cui, Yosky Kataoka, Takumi Satoh, Aya Yamagata, Noriyuki Shirakawa, Yumiko Watanabe, Masaaki Suzuki, Hisato Yanase, Kiyoshi Kataoka, Yasuyoshi Watanabe
    We found a novel subtype of prostaglandin (PG) I2 receptor (IP2) expressed in the central nervous system. Recently we have demonstrated that (15R)-16-m-tolyl-17,18,19,20-tetranorisocarbacyclin (15R-TIC) and 15-deoxy-16-m-tolyl-17,18,19,20-tetranorisocarbacyclin (15-deoxy-TIC), IP2-specific ligands, significantly prevented high (50%) oxygen-induced apoptotic neuronal death in cultured hippocampal neurons. We report here a potent neuroprotective effect of such analogs on delayed neuronal death of hippocampal CA1 neurons following transient ischemia for 3 min in gerbils. (15S)-16-m-tolyl-17,18,19,20-tetranorisocarbacyclin (15S-TIC), which nonselectively acts both on the PGI2 receptor expressed in the peripheral tissue (IP1) and on IP2, also showed a neuroprotective effect on such an ischemic model at higher doses than those for 15R-TIC and 15-deoxy-TIC. These PGI2, analogs did not affect brain temperature, indicating that the agents showed the neuroprotective effect not by a hypothermic effect, but rather by the direct action on neurons.
    Academic Press Inc., 19 Nov. 1999, Biochemical and Biophysical Research Communications, 265(2) (2), 301 - 304, English

  • Takumi Satoh, Yasuyuki Ishikawa, Yosky Kataoka, Yilong Cui, Hisato Yanase, Koichi Kato, Yumiko Watanabe, Kazuhiko Nakadate, Kiyoshi Matsumura, Hiroshi Hatanaka, Kiyoshi Kataoka, Ryoji Noyori, Masaaki Suzuki, Yasuyoshi Watanabe
    Prostacyclin (PGI2) is a critical regulator of the cardiovascular system, via dilatation of vascular smooth muscle and inhibition of platelet aggregation. Our previous studies demonstrated that a novel subtype of PGI2 receptor, which is clearly distinct from a peripheral subtype in terms of ligand specificity, is expressed in the rostral region of the brain, e.g. cerebral cortex, hippocampus, thalamus and striatum, and that (15R)-16-m-17,18,19,20-tetranorisocarbacyclin (15R-TIC) and 15-deoxy-16-m-17,18,19,20-tetranorisocarbacyclin (15-deoxy-TIC) specifically bind to the central nervous system (CNS)-specific PGI2 receptor. Here, we report that these CNS-specific PGI2 receptor ligands, including PGI2 itself, prevented the neuronal death. They prevented apoptotic cell death of hippocampal neurons induced by high (50%) oxygen atmosphere xanthine+xanthine oxidase, and serum deprivation. IC50s for neuronal death were ~ 30 and 300 nM for 15-deoxy-TIC and 15R-TIC, respectively, which well correlated with the binding potency for the CNS-specific PGI2 receptor. 6-Keto-PGF(1α) (a stable metabolite of PGI2), peripheral nervous system-specific PGI2 ligands and other prostaglandins (PGs) than PGI2 did not show such neuroprotective effects. In vivo, 15R-TIC protected CA1 pyramidal neurons against ischaemic damage in gerbils. These results indicate that CNS-specific PGI2 ligands have neuronal survival-promoting activity both in vitro and in vivo, and may represent a new type of therapeutic drug for neurodegeneration.
    Sep. 1999, European Journal of Neuroscience, 11(9) (9), 3115 - 3124, English

  • YAMADA Hisao, KOMINAMI Shiro, TAKEMORI Shigeki, KITAWAKI Jo, KATAOKA Yosky
    To elucidate the steroid-synthesis in the mammalian brain (i. e., neurosteroid), we immunohistochemically studied various kinds of steroidogenic cytochrome P450 enzymes in the rat brain. The primary antibodies used in this study were rabbit polyclonal antibodies to cholesterol side-chain cleavage (SCC), C21-hydroxylase (C21), 11β-hydroxylase (11β), 17α-hydroxylase/C17-20 lyase (17α) and aromatase (AROM). The immunoreactivities for the microsome enzymes, C21 and 17α were located in the neuronal cell-bodies and proximal parts of their fibers, while mitochondria enzymes, SCC and 11β were located in the cell-bodies and their fibers and terminals. These immunoreactivities were distributed in the limbic structures of prosencephalon including hippocampus and amygdaloid complex, the hypothalamus including preoptic area, the cerebellar cortex, and some of other regions. All the sets of these enzymes did not always coexist in the identical cells, however, in the hypothalamus and cerebellum these enzymes are thought to work one after another in adjacent cells, forming the "steroidogenic cellular circuits". These findings strongly suggest that the steroidsynthesis occurs in the neurons; and the neurosteroids exist in the mammalian brain.
    JAPAN SOCIETY OF HISTOCHEMISTRY AND CYTOCHEMISTRY, 01 Oct. 1997, Acta. Histochem. and Cytochem. 30, 1997, 609-616, 30(5) (5), 609 - 616, English

  • Of known neurotransmitters, glutamate is the most likely to be released from chick cochlear hair cells
    Journal of Neurophysiology 76, 1996, 1870-1879


  • Cell proliferation and renewal of mouse adrenal cortex
    Journal of Anatomy 188, 1996, 375-381

  • Afferent synaptic transmission in hair cells
    Biomedical Research 15, Supplement 1, 1994, 47-49

  • Activation of glutamate receptors in response to membrane depolarization of hair cells isolated from chick cochlea
    Journal of Physiology (London) 477, 1994, 403-414

  • A postsynaptic excitatory amino acid transporter with chloride conductance functionally regulated by neuronal activity in cerebellar Purkinje cells
    The Journal of Neuroscience 17, 1997, 7017-7024

■ Affiliated Academic Society
  • 日本レーザー治療学会

  • 日本組織細胞化学会

  • 日本生理学会

  • 日本疲労学会

  • 日本神経科学会

  • 北米神経科学会

  • Society for Neuroscience

  • Physiological Society of Japan

  • Japan Neuroscience Society

■ Research Themes
  • 光技術を用いた脳機能制御
    Competitive research funding

  • 中枢神経機能再編
    Competitive research funding

  • 疲労感誘発のメカニズム
    Competitive research funding

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