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Neurophysiological study for excitatory amino acids-induced neurotoxicity and apoptosis in cultured retinal neurons.

Research Project

Project/Area Number 09671801
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Ophthalmology
Research InstitutionHIROSHIMA UNIVERSITY

Principal Investigator

MISHIMA Hiromu  Faculty of Medicine, Professor, 医学部, 教授 (20034100)

Co-Investigator(Kenkyū-buntansha) MINAMOTO Atushi  Facalty of Medicine, Assistant Professor, 医学部, 講師 (10253072)
広田 篤  広島大学, 附属病院, 助手 (10243560)
Project Period (FY) 1997 – 1998
Project Status Completed (Fiscal Year 1998)
Budget Amount *help
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1998: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1997: ¥2,600,000 (Direct Cost: ¥2,600,000)
Keywordsglutamate / VIP / PACAP / retinal ganglion cell / magnetic cell sorter / Thy-1 / 細胞培養 / 逆行性標識 / 培養網膜 / 神経細胞死
Research Abstract

1. Protection of vasoactive intestinal peptide (VIP) against glutamate-induced neurotoxicity in cultured retinal neurons.
VIP (10 nM - 1 muM) was attenuated glutamate-induced neurotoxicity in a concentration-dependent manner. This protective effect was antagonized by VIP6-28, a VIP recptor antagonist, and H-89, a protein kinase A (PKA) inhibitor. VIP did not affect glutamate-induced current and Ca^<2+> influx. VIP is suggested to act as a protective factor against glutamate-induced neurotoxicity of retinal neurons by elevating the cAMP level via VIP receptors. Activated PKA might have an effect downstream of the Ca^<2+> influx in glutamate neurotoxicity.
2. Protection of pituitary adenylate cyclase activating peptide (PACAP) against glutamate-induced neurotoxicity in cultured retinal neurons.
PACAP27 (10 nM - 1 muM) and PACAP38 (10 nM - 1 muM) were attenuated glutamate-induced neurotoxicity in a concentration-dependent manner. Activation of mitogen activated protein (MAP) kinase by PACAPs was inhibited by H-89. PACAPs are suggested to act as neuroprotective factors against glutamate-induced neurotoxicity by activating MAP kinase, which is due to PKA activation via PACAP receptors.
3. Rat retinal ganglion cells (RGCs) culture enriched with the magnetic cell sorter (MACS).
We demonstrated a new RGC-culture technique using MACS.It enriched RGCs from 0.55 % to 31.0 % of all retinal neurons and enhanced the survival of enriched RGCs for over 2 weeks. The whole-cell patch clamp evaluation was suggested that three ionotropic glutamate receptor subtypes such as NMDA, kainate and AMIPA receptors existed on MACS-separated RGCs. This culture system is thought to be an appropriate model for studying glutamate-induced neurotoxicity in RGC.

Report

(3 results)
  • 1998 Annual Research Report   Final Research Report Summary
  • 1997 Annual Research Report
  • Research Products

    (5 results)

All Other

All Publications (5 results)

  • [Publications] Keisuke Shoge: "Protective effects vasoactive intestinal peptide against delayed glutamate neurotoxicity in cultured retina." Brain Research. 809. 127-136 (1998)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1998 Final Research Report Summary
  • [Publications] Keisuke Shoge: "Rat retinal ganglion cells culture enriched with the magnetic cell sorter." Neuroscinece Letters. 259. 111-114 (1999)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1998 Final Research Report Summary
  • [Publications] Shoge, K.: "Protective effects of vasoactive intestinal peptide against delayd glutamate neurotoxicity in cultured reina." Brain Research. 809. 127-136 (1998)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1998 Final Research Report Summary
  • [Publications] Shoge, K.: "Rat retinal ganglion cells culture enriched with the magnetic cell sorter." Neuroscience Letters. 259. 111-114 (1999)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1998 Final Research Report Summary
  • [Publications] Keisuke Shoge: "Rat retinal ganglion cells culture enriched with the magnetic cell sorter." Neuroscinece Letters. 259. 111-114 (1999)

    • Related Report
      1998 Annual Research Report

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

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