Central and systemic morphine-induced antinociception in mice: contribution of descending serotonergic and noradrenergic pathways.
Central and systemic morphine-induced antinociception in mice: contribution of descending serotonergic and noradrenergic pathways.
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发表时间：
1987-07
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通讯作者：
S. Wigdor;George L. Wilcox
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作者：
S. Wigdor;George L. Wilcox
在小鼠中检查了下行的肾上腺素能和去甲肾上腺素能通路对脊髓上和全身给予硫酸吗啡的抗伤害性作用的相对重要性，以及脊髓上和脊髓上给予吗啡之间观察到的抗伤害性协同作用。静脉注射吗啡，鞘内（i.t.），S.C.或i.t. + i. c. v.产生剂量依赖性抗伤害感受反应，如通过甩尾试验所测量的。吗啡（i. c. v.）显著向右移动了相等的i.t.剂量的麦角新碱或酚妥拉明。然而，最明显的向右移动是由i.t.施用选择性α-2拮抗剂育亨宾。给药亚镇痛剂量的吗啡（i.t.）沿着吗啡（i. c. v.）移动吗啡（i. c. v.）6-向左折叠。得到的吗啡（i. c. v.）酚妥拉明（i.t.）而不是通过麦角新碱（i.t.）。类似地，吗啡（s.c.）酚妥拉明（i.t.）而不是通过麦角新碱（i.t.）。这些结果表明，下降的去甲肾上腺素能系统，比肾上腺素能系统，可能是一个重要的组成部分，在脊髓/脊髓上的相互作用机制，可能介导的镇痛作用，全身给药吗啡。
The relative importance of descending serotonergic and noradrenergic pathways to the antinociceptive action of supraspinally and systemically administered morphine sulfate, and to the antinociceptive synergism observed between spinally and supraspinally administered morphine was examined in mice. Morphine administered i.c.v., intrathecally (i.t.), s.c. or i.t. + i.c.v. produced a dose-dependent antinociceptive response, as measured by the tail-flick test. The dose-response curve for morphine (i.c.v.) was shifted significantly to the right by equal i.t. doses of methysergide or phentolamine. However, the most pronounced shift to the right was caused by i.t. administration of the selective alpha-2 antagonist yohimbine. Administration of a subantinociceptive dose of morphine (i.t.) along with morphine (i.c.v.) shifted the dose-response curve for morphine (i.c.v.) 6-fold to the left. The resulting dose-response curve for morphine (i.c.v.) was shifted to the right more by phentolamine (i.t.) than by methysergide (i.t.). Similarly, the dose-response curve for morphine (s.c.) was shifted more to the right by phentolamine (i.t.) than by methysergide (i.t.). These results suggest that the descending noradrenergic system, more than the serotonergic system, may be an important component in spinal/supraspinal interactive mechanisms that may mediate the antinociceptive action of systemically administered morphine.