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+ (KATP) 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 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 μ-opioid receptor functions, which subsequently leads to the inhibition of FS-SIA since antinociception is produced by the activation of μ-receptors.
