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

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Author(s)

    • 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

Abstract

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.

Journal

  • The Japanese Journal of Pharmacology

    The Japanese Journal of Pharmacology 71(3), 269-272, 1996-07

    The Japanese Pharmacological Society

References:  14

Codes

  • NII Article ID (NAID)
    10008189131
  • NII NACSIS-CAT ID (NCID)
    AA00691188
  • Text Lang
    ENG
  • Article Type
    SHO
  • ISSN
    00215198
  • Data Source
    CJP  J-STAGE 
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