The role of dopamine receptors in ventrolateral orbital cortex-evoked antinociception in a rat formalin test model
The role of dopamine receptors in ventrolateral orbital cortex-evoked antinociception in a rat formalin test model
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多巴胺受体在大鼠福尔马林测试模型中腹外侧眶皮层诱发的抗伤害作用中的作用。
DOI：
10.1016/j.ejphar.2011.01.064
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发表时间：
2011-04-25
影响因子：
5
通讯作者：
Chen, Teng
中科院分区：
文献类型：
--
作者：
Dang, Yong-Hui;Xing, Bo;Chen, Teng
本研究探讨了多巴胺和D-1和D-2样多巴胺受体在持续性炎性痛大鼠腹外侧眶皮层（VLO）诱发的抗伤害感受中的作用。在大鼠单侧后爪垫注射福尔马林后，观察腹外侧核（VLO）内微量注射多巴胺受体激动剂和拮抗剂对伤害性行为的影响。结果表明，VLO微量注射非选择性多巴胺受体激动剂阿扑吗啡（R（-）-阿扑吗啡盐酸盐，1.0，2.5和5.0 μ g）抑制福尔马林注射诱导的晚期伤害性行为;这种作用被D-2样多巴胺受体拮抗剂S（-）-雷氯必利（+）-酒石酸盐减弱（雷氯必利，3.0 μ g），但不受D-1样多巴胺受体拮抗剂R（+）-SCH-23390盐酸盐（SCH-23390，1.0 μ g）的影响。阿扑吗啡诱导的抗伤害感受通过向相同的VLO部位微量注射D-2样多巴胺受体激动剂盐酸（-）-喹吡罗（2.0和5.0 μ g）来模拟，并且这种作用被雷氯必利（3.0 μ g）拮抗。此外，微量注射D-1样多巴胺受体激动剂R（+）-SKF-38393盐酸盐（5.0 μ g）在后期对福尔马林诱导的伤害性行为没有影响。然而，D-1样多巴胺受体拮抗剂SCH-23390（2.5、5.0和10 μ g）以剂量依赖性方式抑制伤害性行为。这些结果表明，在持续性炎性痛模型中，多巴胺通过不同的机制介导VLO诱导的抗伤害性感受; D-2样受体介导多巴胺诱导的抗伤害性感受，而D-1样多巴胺受体对伤害性感受行为表现出紧张性易化作用，因此阻断D-1样多巴胺受体可诱导抗伤害性感受。(C)2011爱思唯尔有限公司版权所有。
The present study examined the roles of dopamine and D-1- and D-2-like dopamine receptors in ventrolateral orbital cortex (VLO)-evoked antinociception in rats with persistent inflammatory pain. Following formalin injection into the rat unilateral hindpaw pad, the effects of dopamine receptor agonist and antagonist microinjections into the VLO on nociceptive behavior were observed. Results demonstrated that VLO microinjection of the non-selective dopamine receptor agonist apomorphine (R(-)-apomorphine hydrochloride, 1.0, 2.5 and 5.0 mu g) depressed later-phase nociceptive behavior induced by formalin injection; this effect was attenuated by the D-2-like dopamine receptor antagonist S(-)-raclopride(+)-tartrate salt (raclopride, 3.0 mu g), but not by the D-1-like dopamine receptor antagonist R(+)-SCH-23390 hydrochloride (SCH-23390, 1.0 mu g). Apomorphine-induced antinociception was mimicked by microinjection of the D-2-like dopamine receptor agonist (-)-quinpirole hydrochloride (2.0 and 5.0 mu g) into the same VLO site, and this effect was antagonized by raclopride (3.0 mu g). In addition, microinjection of the D-1-like dopamine receptor agonist R(+)-SKF-38393 hydrochloride (5.0 mu g) had no effect on formalin-induced nociceptive behavior during the later phase. However, the D-1-like dopamine receptor antagonist SCH-23390 (2.5, 5.0 and 10 mu g) depressed nociceptive behavior in a dose-dependent manner. These results suggested that dopamine mediated VLO-induced antinociception via different mechanisms in the persistent inflammatory pain model; D-2-like receptors mediated dopamine-induced antinociception, while D-1-like dopamine receptors exhibited tonic facilitatory action on nociceptive behavior, thereby blocking D-1-like dopamine receptors could induce antinociception. (C) 2011 Elsevier B.V. All rights reserved.