Involvement of Complexin II in Synaptic Plasticity in the CA1 Region of the Hippocampus: The Use of Complexin II-Lacking Mice

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An electrophysiological study was performed with mice lacking complexin II, a presynaptic protein.The long−term potentiation(LTP)by high−frequency stimulation, recorded in the hippocampal CA1 area, was decreased in complexin II−lacking mice(CPXII KO mice).The overall postsynaptic currents elicited by low frequency stimulation on the Schaffer collateral/commissural fibers in the hippocampal CA1 pyramidal cells were not different between wild−type and mutant mice.Excitatory postsynaptic currents(EPSCs)recorded in the presence of 50μM bicuculline and inhibitory postsynaptic currents(IPSCs)recorded in the presence of 50μM AP−5(DL−2−amino−5−phosphonopentanoic acid)+ 30μM CNQX(6−cyano−7−nitroquinoxaline−2, 3−dione)were also identical between wild−types and mutants.Furthermore, the EPSCs following repetitive stimulation(10 Hz)in CPXII KO mice did not show any difference with wild−types.These findings suggest that complexin II does not play a crucial role in ordinary neural transmission, short−term synaptic plasticity or synaptic transmission during high−frequency repetitive stimulation.Therefore, the protein is thought to be involved in the LTP process following tetanic stimulation, including the induction and /or maintenance of the LTP.

収録刊行物

  • The Japanese journal of pharmacology

    The Japanese journal of pharmacology 84(2), 179-187, 2000-10-01

    公益社団法人 日本薬理学会

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各種コード

  • NII論文ID(NAID)
    10008185707
  • NII書誌ID(NCID)
    AA00691188
  • 本文言語コード
    ENG
  • 資料種別
    ART
  • ISSN
    00215198
  • NDL 記事登録ID
    5549357
  • NDL 雑誌分類
    ZS51(科学技術--薬学)
  • NDL 請求記号
    Z53-D199
  • データ提供元
    CJP書誌  NDL  J-STAGE 
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