Open AccessImplication of ATP-Sensitive K+ Channels in Various Stress-Induced Analgesia (SIA) in Mice
Author(s) -
Kaoru Nakao,
Masakatsu Takahashi,
Hiroshi Kaneto
Publication year - 1996
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.71.269
Subject(s) - glibenclamide , chemistry , pharmacology , cromakalim , receptor , nociception , endocrinology , medicine , agonist , biology , biochemistry , diabetes mellitus
Exposure to footshock (2 mA, 1-sec duration, 0.2 Hz for 15 min; FS), forced swimming (water at 20 degrees C for 3 min, SW) or psychological stress (using a communication box for 5 min, PSY) produced antinociceptive effects (stress-induced analgesia, SIA). Intracerebroventricular (i.c.v.) injection of glibenclamide (10-40 micrograms/mouse), an ATP-sensitive K+ (KATP) channel blocker, antagonized FS-SIA, while SW- and PSY-SIA were unaffected by the compound. Cromakalim (0.1-10 micrograms/mouse, i.c.v.), a KATP-channel opener, did not affect FS-, SW- or PSY-SIA. Thus, we provided evidence that central KATP channels participate in the production of FS-SIA but not production of SW- or PSY-SIA; and we suggest that glibenclamide, through closing of KATP channels, suppresses mu-opioid receptor functions, which subsequently leads to the inhibition of FS-SIA since antinociception is produced by the activation of mu-receptors.