Department of Anesthesiology and Pain Medicine, Chonnam National University, Medical School, Gwangju, Republic of Korea.
Neurosci Lett. 2013 May 10;542:118-22. doi: 10.1016/j.neulet.2013.03.026. Epub 2013 Mar 29.
The purpose of this study was to examine the effects of intrathecal nociceptin for neuropathic pain and determine the role of spinal opioid receptor types. Neuropathic pain was induced by ligation of L5 and L6 spinal nerves in male Sprague-Dawley rats. Several antagonists were intrathecally administered to evaluate the action mechanisms of nociceptin: nonselective opioid receptor antagonist (naloxone), μ opioid receptor antagonist (CTOP), δ opioid receptor antagonist (naltrindole) and κ opioid receptor antagonist (GNTI). The levels of opioid receptor proteins were examined by Western blotting. Intrathecal nociceptin produced dose-dependent antiallodynia. Intrathecal naloxone reversed the antinociception of nociceptin. Intrathecal CTOP, naltrindole and GNTI reversed the antinociceptive effect of nociceptin. Western blots showed that the levels of spinal opioid receptor proteins did not differ between rats with neuropathic pain and naïve rats. Intrathecal nociceptin increased the level of δ opioid receptor protein compared with that of nerve ligated rats, while the levels of μ, and κ opioid receptor proteins were unchanged. These results suggest that intrathecal nociceptin produced antiallodynic effect in spinal nerve ligation-induced neuropathic pain. All three types of spinal μ, δ, and κ opioid receptors were involved in the antiallodynic mechanism of nociceptin.
本研究旨在探讨鞘内给予孤啡肽对神经病理性疼痛的影响，并确定脊髓阿片受体类型的作用。通过结扎雄性 Sprague-Dawley 大鼠的 L5 和 L6 脊神经诱导神经病理性疼痛。鞘内给予几种拮抗剂以评估孤啡肽的作用机制：非选择性阿片受体拮抗剂（纳洛酮）、μ 阿片受体拮抗剂（CTOP）、δ 阿片受体拮抗剂（naltrindole）和 κ 阿片受体拮抗剂（GNTI）。通过 Western blot 检测阿片受体蛋白水平。鞘内给予孤啡肽产生剂量依赖性抗痛觉过敏。鞘内给予纳洛酮逆转孤啡肽的镇痛作用。鞘内给予 CTOP、naltrindole 和 GNTI 逆转孤啡肽的镇痛作用。Western blot 显示，神经结扎大鼠与未处理大鼠的脊髓阿片受体蛋白水平没有差异。与神经结扎大鼠相比，鞘内孤啡肽增加了 δ 阿片受体蛋白的水平，而 μ 和 κ 阿片受体蛋白的水平没有变化。这些结果表明，鞘内孤啡肽在脊神经结扎诱导的神经病理性疼痛中产生抗痛觉过敏作用。脊髓 μ、δ 和 κ 三种阿片受体都参与了孤啡肽的抗痛觉过敏机制。
