一過性脳虚血と海馬長期増強 Transient cerebral ischemia and long-term potentiation in the rat hippocampus

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Long-term potentiation (LTP) has been widely studied as a form of synaptic plasticity that represents a cellular mechanism of learning and memory. Among numerous processes and molecules that may be involved in LTP formation, a great many of them including neurotrophic and transcription factors have been described as those involved in neural death after ischemic insult. Nitric oxide (NO) is a molecule that is known to also exert double-edged effects on LTP formation. Here we will be describing recent advances with respect to the LTP mechanisms in the hippocampal synapses, a critical brain region for learning and memory function. In another context, we described our study elucidating the changes in hippocampal LTP as a functional response to transient cerebral ischemic insult, from the viewpoint of its relevance to NO production. As indices of NO production, nitrite and nitrate levels were determined by in vivo microdialysis. It was demonstrated that hippocampal LTP deficiency after transient cerebral ischemia was preceded by an increase in hippocampal NO production. Direct or indirect inhibition of an inducible NO synthase restored ischemia-induced LTP deficiency. These findings suggest that NO production, in part via inducible NO synthase, is responsible for LTP deficiency after transient cerebral ischemia in the rat hippocampus.

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  • 日本薬理学雑誌

    日本薬理学雑誌 111(1), 55-63, 1998-01-01

    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)
    10008182087
  • NII書誌ID(NCID)
    AN00198335
  • 本文言語コード
    JPN
  • 資料種別
    REV
  • ISSN
    00155691
  • NDL 記事登録ID
    4382498
  • NDL 雑誌分類
    ZS51(科学技術--薬学)
  • NDL 請求記号
    Z19-247
  • データ提供元
    CJP書誌  NDL  J-STAGE 
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