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Effect of neuropeptideY on the T-type Ca^<2+> channel current

Research Project

Project/Area Number 15500254
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Neurochemistry/Neuropharmacology
Research InstitutionKansai Medical University (2004)
Niigata University (2003)

Principal Investigator

OKADA Masayoshi  Kansai Medical University, Faculty of Medicine, Assistant professor, 医学部, 講師 (40334677)

Co-Investigator(Kenkyū-buntansha) 樋口 宗史  新潟大学, 大学院・医歯学総合研究科, 教授 (30150337)
山口 剛  新潟大学, 大学院・医歯学総合研究科, 助手 (70323970)
Project Period (FY) 2003 – 2004
Project Status Completed (Fiscal Year 2004)
Budget Amount *help
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2004: ¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2003: ¥600,000 (Direct Cost: ¥600,000)
KeywordsT-type Ca^<2+>_channel / neuropeptideY / patch-clamp technique / RT-PCR / NG108-15 cell / hippocampal slice / ラット海馬 / スライス培養 / スライスパッチクランプ / 電位依存性電流 / ホールセル記録 / NPY受容体
Research Abstract

T-type Ca^<2+> channel plays pivotal roles in regulating the excitability of the neurons and non-neuronal excitable cells. The neuropeptideY (NPY) is one of the most abundantly expressed neuropeptides in the central and peripheral nervous systems, and its distribution correlates well with that of T-type Ca^<2+> channel, suggesting a functional interaction with it. The aim of this study was to investigate the functional interaction. In the former half of this study, I used the undifferentiated NG108-15 cells, in which the expression of the T-type Ca^<2+> channel current was confirmed. I found that low doses of NPY significantly augmented the T-type Ca^<2+> channel current with whole cell patch-clamp technique using Ba^<2+> as the charge carrier. The NPY treatment shifted the I-V relationship negatively. Experiments using NPY receptor subtype-selective agonist/antagonists revealed that both Y_1 and Y_2 receptors additively involved in the augmentation of the current. Consistently, RT-PCR analysis showed the expressions of mRNAs for Y_1 and Y_2 receptors. In the later half, to investigate the functional interaction, which was shown in the NG 108-15 cells, in the brain preparation, I set up culture system of hippocampal slice, which was reported to express the proteins. I examined the voltage-dependent channel currents expressed in the CA1 pyramidal neurons with slice patch-clamp technique. Further work is needed to obtain the conclusion of the NPY's effect on the voltage-dependent channel currents.

Report

(3 results)
  • 2004 Annual Research Report   Final Research Report Summary
  • 2003 Annual Research Report
  • Research Products

    (3 results)

All 2004 Other

All Journal Article (2 results) Publications (1 results)

  • [Journal Article] Effect of neuropeptideY on the T-type Ca^<2+> channel current expressed in NG1-8015 cells2004

    • Author(s)
      Okada M, Hasagawa A, Higuchi H
    • Journal Title

      Acta Medica et Biologica 52

      Pages: 103-110

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2004 Final Research Report Summary
  • [Journal Article] Effect of neuropeptideY on the T-type Ca2+ channel current expressed in NG1-8015 cells2004

    • Author(s)
      Okada M, Hasagawa A, Higuchi H
    • Journal Title

      Acta Medica et Biologica 52

      Pages: 103-110

    • Related Report
      2004 Annual Research Report
  • [Publications] Masayoshi Okada, Gabriel Corfas: "Neuregulin1 downregulates postsynaptic GABAA receptors at the hippocamp1 Inhibitory synapse"Hippocampus. (出版予定). (2004)

    • Related Report
      2003 Annual Research Report

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Published: 2003-04-01   Modified: 2016-04-21  

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