Division of Physiology, Department of Basic sciences, Faculty of Veterinary Medicine, Urmia University, Urmia, Iran.
Division of Physiology, Department of Basic sciences, Faculty of Veterinary Medicine, Urmia University, Urmia, Iran.
Eur J Pharmacol. 2015 Jul 5;758:147-52. doi: 10.1016/j.ejphar.2015.04.002. Epub 2015 Apr 9.
Nicotinic acetylcholine and opioid receptors are involved in modulation of pain. In the present study, we investigated the effects of microinjection of nicotinic acetylcholine and opioid compounds into the ventral orbital cortex (VOC) on the formalin-induced orofacial pain in rats. For this purpose, two guide cannulas were placed into the left and right sides of the VOC of the brain. Orofacial pain was induced by subcutaneous injection of a diluted formalin solution (50μl, 1.5%) into the right vibrissa pad and face rubbing durations were recorded at 3-min blocks for 45min. Formalin produced a marked biphasic pain response (first phase: 0-3min and second phase: 15-33min). Epibatidine (a nicotinic receptor agonist) at doses of 0.05, 0.1 and 0.2μg/site, morphine (an opioid receptor agonist) at doses of 0.5, 1 and 2μg/site and their sub-analgesic doses (0.025μg/site epibatidine with 0.25μg/site morphine) combination treatment suppressed the second phase of pain. The antinociceptive effect induced by 0.2μg/site of epibatidine, but not morphine (2μg/site), was prevented by 2μg/site of mecamylamine (a nicotinic receptor antagonist). Naloxone (an opioid receptor antagonist) at a dose of 2μg/site prevented the antinociceptive effects induced by 2μg/site of morphine and 0.2μg/site of epibatidine. No above-mentioned chemical compounds affected locomotor activity. These results showed that at the VOC level, epibatidine and morphine produced antinociception. In addition, opioid receptor might be involved in epibatidine-induced antinociception, but the antinociception induced by morphine was not mediated through nicotinic acetylcholine receptor.
烟碱型乙酰胆碱和阿片受体参与疼痛的调制。在本研究中，我们研究了将烟碱型乙酰胆碱和阿片化合物微注射到眶下皮质（VOC）对大鼠福尔马林诱导的口腔疼痛的影响。为此，将两个引导套管放置到大脑左、右侧的 VOC 中。口腔疼痛通过将稀释的福尔马林溶液（50μl，1.5%）皮下注射到右侧触须垫中诱导，并在 45 分钟内以 3 分钟为间隔记录面部摩擦持续时间。福尔马林产生明显的双相疼痛反应（第一相：0-3 分钟，第二相：15-33 分钟）。烟碱型乙酰胆碱受体激动剂 epibatidine（剂量为 0.05、0.1 和 0.2μg/部位）、阿片受体激动剂吗啡（剂量为 0.5、1 和 2μg/部位）及其亚镇痛剂量（0.025μg/部位 epibatidine 与 0.25μg/部位吗啡）联合治疗抑制了疼痛的第二相。0.2μg/部位的 epibatidine 诱导的镇痛作用，但不是吗啡（2μg/部位），被 2μg/部位的美加明（烟碱型乙酰胆碱受体拮抗剂）所阻止。阿片受体拮抗剂纳洛酮（剂量为 2μg/部位）阻止了 2μg/部位的吗啡和 0.2μg/部位的 epibatidine 诱导的镇痛作用。上述化学化合物均未影响运动活动。这些结果表明，在 VOC 水平上，epibatidine 和吗啡产生了镇痛作用。此外，阿片受体可能参与了 epibatidine 诱导的镇痛作用，但吗啡诱导的镇痛作用不是通过烟碱型乙酰胆碱受体介导的。
