ATP-sensitive potassium channels mediate norepinephrine- and morphine-induced antinociception at the spinal cord level

The effects of intrathecally (i.t.) administered glibenclamide, a blocker of adenosine triphosphate-senstrive potassium (K(ATP)) channels, on antinociception produced by i.t. norepinephrine, morphine, or 5'N-ethylcarboxamide adenosine, an adenosine agonist, were investigated using tail-flick assay. The results showed that: 1) i.t. norepinephrine (1 nmol), morphine (0.5 nmol) and 5'-N-ethylcarboxamide adenosine (0.5 nmol) elicited prolongation of tail-flick latency, 2) i.t. glibenclamide given in 2 different doses (5 and 10 nmol) exhibited no effects on tail-flick latency, 3) the antinociception produced by norepinephrine (1 nmol) and morphine (0.5 nmol) was blocked by glibenclamide in a dose-dependent manner, 4) glibenclamide failed to modulate the effects of 5'-N-ethylcarboxamide adenosine on tailflick latency. These observations suggest that K(ATP) channels may play an important role in norepinephrine- and/or morphine-induced antinociception at the spinal level.