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• W2024841609 abstract "Glibenclamide is one of the most potent sulfonylurea-derived antidiabetic durgs which block the adenosine triphosphate-sensitive potassium (KATP) channels. In the present study, we found that none of morphine, U-50, 488H (a selective κ agonist) and baclofen (a selective GABAB agonist) added to the incubation medium at concentrations up to 10−4 M had appreciable effect on the specific binding of [ [cyclohexyl-2,3-3H(N)]glibenclamide ([3H]glibenclamide) to the isolated mouse brain microsomes. The analgesic activity induced by intracerebroventricular injection (i.c.v.) of morphine but not U-50,488H was antagonized by pretreatment with either i.c.v. glibenclamide or β-funaltrexamine (β-FNA; a selective μ antagonist) in mice. Furthermore, the increasing effect of i.c.v. morphine on the spinal noradrenaline (NA) turnover was greatly antagonized by i.c.v. pretreatment with either β-FNA or glibenclamide. From these results, we demonstrated that KATP channels play an important role as indirect modulators of the supraspinal analgesia induced by μ agonist but not κ agonist in mice and the activation of descending noradrenergic system induced by i.c.v. morphine appears to be suppressed by the blockade of KATP channels." @default.
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• W2024841609 date "1992-11-01" @default.
• W2024841609 modified "2023-09-25" @default.
• W2024841609 title "Role of central ATP-sensitive potassium channels in the analgesic effect and spinal noradrenaline turnover-enhancing effect of intracerebroventricularly injected morphine in mice" @default.
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• W2024841609 doi "https://doi.org/10.1016/0006-8993(92)91549-t" @default.
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