Implication of ATP-Sensitive K^+ Channels in Various Stress-Induced Analgesia (SIA) in Mice

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著者

    • NAKAO Kaoru
    • Department of Pharmacology, Faculty of Pharmaceutical Sciences, Nagasaki University
    • TAKAHASHI Masakatsu
    • Department of Pharmacology, Faculty of Pharmaceutical Sciences, Nagasaki University
    • KANETO Hiroshi
    • Department of Pharmacology, Faculty of Pharmaceutical Sciences, Nagasaki University

抄録

Exposure to footshock (2 mA, 1-sec duration, 0.2 Hz for 15 min; FS), forced swimming (water at 20°C for 3 min, SW) or psychological stress (using a communication box for 5 min, PSY) produced antinociceptive effects (stress-induced analgesia, S1A). Intracerebroventricular (i.c.v.) injection of glibenclamide (10-40 μg/mouse), an ATP-sensitive K<SUP>+</SUP> (K<SUB>ATP</SUB>) channel blocker, antagonized FS-SIA, while SW- and PSY-SIA were unaffected by the compound. Cromakalim (0.1-10 μg/mouse, i.c.v.), a K<SUB>ATP</SUB>-channel opener, did not affect FS-, SW- or PSY-SIA. Thus, we provided evidence that central K<SUB>ATP</SUB> channels participate in the production of FS-SIA but not production of SW or PSY-SIA; and we suggest that glibenclamide, through closing of K<SUB>ATP</SUB> channels, suppresses μ-opioid receptor functions, which subsequently leads to the inhibition of FS-SIA since antinociception is produced by the activation of μ-receptors.

収録刊行物

  • The Japanese journal of pharmacology

    The Japanese journal of pharmacology 71(3), 269-272, 1996-07

    The Japanese Pharmacological Society

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各種コード

  • NII論文ID(NAID)
    10008189131
  • NII書誌ID(NCID)
    AA00691188
  • 本文言語コード
    ENG
  • 資料種別
    SHO
  • ISSN
    00215198
  • データ提供元
    CJP書誌  J-STAGE 
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