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The involvement of phosphatidylinositol system in a rat model of schizophrenia

Research Project

Project/Area Number 21591526
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Psychiatric science
Research InstitutionNara Medical University

Principal Investigator

NORIYAMA Yoshinobu  奈良県立医科大学, 精神医学, 研究員 (20305725)

Co-Investigator(Kenkyū-buntansha) 岸本 年史  奈良県立医科大学, 医学部, 教授 (60201456)
小川 陽一  奈良県立医科大学, 医学部, 助教 (10201394)
Project Period (FY) 2009 – 2011
Project Status Completed (Fiscal Year 2011)
Budget Amount *help
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2011: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Keywords統合失調症 / フォスファチジルイノシトール / ドパミン / PI-PLC / social isolation / 生理学 / 脳・神経
Research Abstract

First we examined the effect of SKF83959, Phosphatidylinositol-linked D1 receptor agonist, on synaptic transmission in CA1 area of mouse hippocampus. Spontaneous inhibitory postsynaptic currents recorded on pyramidal cells was enhanced by SKF83959.Then we decided to utilize'social isolation model'(SI-model) mice as a schizophrenia animal model. In behavioral tests, the reduction of prepulse inhibition and the decrease of percent alteration in Y-maze task were revealed, and we accepted these mice as schizophrenia animal model. Next we performed the electrophysiological recording to clarify certain abnormalities in a local neural circuit of SI-model mice. We recorded excitatory postsynaptic currents(EPSCs) and inhibitory postsynaptic currents(IPSCs) from pyramidal cells in layer 5 of mouse prefrontal cortex. The frequencies of the both spontaneous EPSCs and miniature EPSCs were lower in SI-model mice than control mice, whereas there was no significant difference between SI-model and control in spontaneous IPSCs. However, as we hypothesize alterations of the excitability of GABAergic interneurons, we next plan to directly record from interneurons to detect alterations of the membrane property. Following the comprehensive identification of the abnormalities of neural circuits in SI-model mouse, we plan to examine the therapeutic response of chronic administration of SKF83959 against aberrant neural circuits in SI-model mice PFC.

Report

(4 results)
  • 2011 Annual Research Report   Final Research Report ( PDF )
  • 2010 Annual Research Report
  • 2009 Annual Research Report
  • Research Products

    (4 results)

All 2010 2009

All Journal Article (2 results) Presentation (2 results)

  • [Journal Article] 興奮性・抑制性シナプス伝達に対するドパミンの効果2009

    • Author(s)
      法山良信
    • Journal Title

      脳と精神の医学

      Volume: 20 Pages: 339-346

    • NAID

      10028262851

    • Related Report
      2011 Final Research Report
  • [Journal Article] 興奮性・抑制性シナプス伝達に対するドパミンの効果2009

    • Author(s)
      法山良信
    • Journal Title

      脳と精神の医学 20

      Pages: 339-346

    • NAID

      10028262851

    • Related Report
      2009 Annual Research Report
  • [Presentation] 新生マウス海馬でのドパミンによるGABA作動性介在性ニューロンの興奮性の増強2010

    • Author(s)
      中川恵樹
    • Organizer
      奈良精神神経科学懇話会
    • Place of Presentation
      奈良県新公会堂
    • Related Report
      2011 Final Research Report 2009 Annual Research Report
  • [Presentation] Enhancement of GABAergic interneuron excitability by dopamine in neonatal mouse hippocampus2009

    • Author(s)
      K. Nakagawa, Y. Ogawa, H. Yoshino, Y. Noriyama, et al.
    • Organizer
      The 36^<th> Congress of the International Union of Physiological Sciences
    • Place of Presentation
      Kyoto
    • Related Report
      2011 Final Research Report

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Published: 2009-04-01   Modified: 2016-04-21  

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