z-logo
open-access-imgOpen Access
Implication 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 -
the 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.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom