Fig. 5. Effects of intrathecal administered tetraethylammonium (TEA), 4-aminopyridine (4-AP), and glibenclamide (Glib) on R-PIA–induced antinociception. (  A and  B ) Intrathecal pretreatment with 5 nmol 4-AP or 100 nmol tetraethylammonium reduced R-PIA–induced antinociception, indicating the involvement of different potassium channels in this process (  P < 0.05 ; vs. pre). (  C –F ) Intrathecal pretreatment with glibenclamide produced a dose-dependent reduction of R-PIA–induced hypoalgesia, indicating that adenosine triphosphate–sensitive potassium channels are partially involved in A1adenosine receptor–mediated antinociception (  P < 0.05 ; vs. pre) . *P < 0.05  versus 0 min by Friedman and Dunnett test. 

Fig. 5. Effects of intrathecal administered tetraethylammonium (TEA), 4-aminopyridine (4-AP), and glibenclamide (Glib) on R-PIA–induced antinociception. (  A and  B ) Intrathecal pretreatment with 5 nmol 4-AP or 100 nmol tetraethylammonium reduced R-PIA–induced antinociception, indicating the involvement of different potassium channels in this process (  P < 0.05 ; vs. pre). (  C F ) Intrathecal pretreatment with glibenclamide produced a dose-dependent reduction of R-PIA–induced hypoalgesia, indicating that adenosine triphosphate–sensitive potassium channels are partially involved in A1adenosine receptor–mediated antinociception (  P < 0.05 ; vs. pre) . *P < 0.05  versus 0 min by Friedman and Dunnett test. 

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