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Histochemical and physiological study of delayd neuronal death

Research Project

Project/Area Number 08671608
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Cerebral neurosurgery
Research InstitutionJichi Medical School

Principal Investigator

OGURO Keiji  Jichi Medical School, Assistant Professor, 医学部, 講師 (90231232)

Co-Investigator(Kenkyū-buntansha) MASUZAWA Toshio  Jichi Medical School, Professor, 医学部, 教授 (60049038)
KAWAI Nobufumi  Jichi Medical School, Professor, 医学部, 教授 (00073065)
OTA Toshiko  Tsukuba University, Associate Professor, 助教授 (40233134)
Project Period (FY) 1996 – 1997
Project Status Completed (Fiscal Year 1997)
Budget Amount *help
¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1997: ¥700,000 (Direct Cost: ¥700,000)
Keywordscerebral ischemi / gluramate recepto / Ca^<2+>-ATPase / protein kinase C / slice / hippocampus / mongolian gerbi / Ca^+-ATPase / Ca^<2+>-ATPase
Research Abstract

1.Making plasmamembrane Ca^<2+>-ATPase antibody, immunohistochemistry
Using Ca^<2+>-ATPase type II antibody we made a immunohistochemical mapping of that enzyme in normal rat and gerbil brain. In hippocampus, the distribution of the enzyme is similar to that one which we have detected enzymehistochemically. That is, the enzyme is diffusely located on the plasma membrane of pyramidal neurons, axon, dendrite. There is no differences in distributional density between CA1, CA3 and dentate gyrus.
2.Physiological study of gerbil hippocampal slices
We studied N-methyl-D-aspartate (NMDA) receptor-mediated synaptic potentials in CA1 pyramidal neurons using hippocampal slices of the gerbils after transient forebrain ischemia. In the presence of 6-cyanc 7-nitroquinoxaline-2,3-dione (CNQX) and bicucullin, stimulation on Schaffer collateral/commissural fibers induced field excitatory postsynaptic potentials (fEPSP) activated by NMDA receptors. We found that in many slices after ischemia, low frequency … More stimulation (0.1-10Hz) to input fibers caused repeated depression and potentiation of the NMDA-mediated fEPSP.The cyclic changes in fEPSP amplitude were dependent on stimulus frequency, ranging from 0.08 to 2.5 cycle/min. The cyclic changes were blocked by application of 1 bis (o-aminophenoxy) ethane-N,N,N', N'-tetraacety1, tetraacetoxymethy1 ester (BAPTA-AM), a membrane permeable Ca^<2+> chelator, but they were little affected by application of vera-pamil or by reducing Ca^<2+>in bathing solution. Intracellular recordings showed periodic depolarizations of membrane potential synchroniz with depression of EPSP.The cyclic phenomenon was significantly attenuated by application of 1-(5-soquinolinylsulfony1)-2-methylpiperazine (H-7) and K252a, protein kinase C (PKC) antagonist.
These results suggest that stimulus dependent NMDA-receptor activation, medi-ated by PKC,takes place the postischemic CA1 neurons and the cyclic change may reflect abnormal intracellular Ca^<2+> signaling process towards neuronal degeneration re-sulted in periodic membrane depolarization.
3.Potential mapping of the gerbil hippocampus stimulated on the contralateral commisural fibers
We made potential mapping of postischemic gerbil hippocampus by recording EPSP induced by contralateral commisural fiber stimulation. We revealed that CA1 pyramidal neurons are in the hyper excitatory state in the early stage (2-8h) following ischemic insult and LTP is significantly increased in that period compared with the non-ischemic group. This is the first report of the abnormal physiological conditions in the early postischemic period in vivo. Less

Report

(3 results)
  • 1997 Annual Research Report   Final Research Report Summary
  • 1996 Annual Research Report
  • Research Products

    (5 results)

All Other

All Publications (5 results)

  • [Publications] Ogura k, Masuzawa T, Kawai N et al.: "Cyclic changes in NMDA receptor activation in hippocampal CAl neurons after ischemia" Neurosience Research. 29. 273-281 (1997)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1997 Final Research Report Summary
  • [Publications] Oguro K., Masuzawa T., Kawai N et al: "Cyclic changes in NMDA receptor activation in hippocampal CA1 neurons after ischemia" Neuroscience Research. 29. 273-281 (1997)

    • Related Report
      1997 Annual Research Report
  • [Publications] Oguro K,et al.: "Histochemical study of Ca^<2+>-ATPase activity in ischemic CA1 pyramidal neurons in the gerbil hippocampus." Acta Neurropathol Berl. 90. 448-453 (1995)

    • Related Report
      1996 Annual Research Report
  • [Publications] Tsubokawa H,Oguro K,et al: "Single glutamate channels in CA1 pyramidal neurones after transient ischaemia." Neuroreport. 6. 527-533 (1995)

    • Related Report
      1996 Annual Research Report
  • [Publications] Tsubokawa H,Oguro K,et al: "Intracellular inositol 1,3,4,5-tetrakisphosphate enhances the calcium current in hippocampal CA1 neurons of the gerbil after ischemia." J Physiol.(London). 497. 67-78 (1996)

    • Related Report
      1996 Annual Research Report

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Published: 1997-04-01   Modified: 2016-04-21  

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