Yu Shuang Quan, Lundeberg Thomas, Yu Long Chuan
Neurobiology Laboratory, College of Life Sciences, and Center for Brain and Cognitive Science and National Laboratory of Biomembrane and Membrane Biotechnology, Peking University, 100871, Beijing, China.
Brain Res. 2003 Sep 5;983(1-2):13-22. doi: 10.1016/s0006-8993(03)03019-1.
The present study was conducted on rats with inflammation induced by subcutaneous injection of carrageenan into the left hindpaw. Intrathecal administration of oxytocin produced dose-dependent increases in the hindpaw withdrawal latency (HWL) to thermal and mechanical stimulation in rats with inflammation. The antinociceptive effect of oxytocin was blocked by intrathecal administration of atosiban, a selective oxytocin antagonist, indicating that oxytocin receptor mediates oxytocin-induced antinociception in the spinal cord. The oxytocin-induced antinociceptive effect was attenuated by intrathecal administration of the opioid antagonist naloxone, suggesting an involvement of the endogenous opioid system in oxytocin-induced antinociception in the spinal cord of rats with inflammation. Furthermore, the antinociceptive effect of oxytocin was attenuated by intrathecal injections of the mu-receptor antagonist beta-funaltrexamine and the kappa-receptor antagonist nor-binaltorphimine, but not by the delta-receptor antagonist naltrindole, illustrating that mu- and kappa-receptors, but not delta-receptor, are involved in oxytocin-induced antinociception in the spinal cord of rats with inflammation. Moreover, intrathecal administration of atosiban alone induced a hyperalgesia in rats with inflammation, indicating that endogenous oxytocin is involved in the transmission and regulation of nociceptive information in the spinal cord of rats with inflammation. The present study showed that both exogenous and endogenous oxytocin displayed antinociception in the spinal cord in rats with inflammation, and mu- and kappa-receptors were involved in oxytocin-induced antinociception.
本研究在通过向大鼠左后爪皮下注射角叉菜胶诱导炎症的大鼠身上进行。鞘内注射催产素可使炎症大鼠对热刺激和机械刺激的后爪缩足潜伏期（HWL）呈剂量依赖性增加。鞘内注射选择性催产素拮抗剂阿托西班可阻断催产素的抗伤害感受作用，表明催产素受体介导了脊髓中催产素诱导的抗伤害感受。鞘内注射阿片类拮抗剂纳洛酮可减弱催产素诱导的抗伤害感受作用，提示内源性阿片系统参与了炎症大鼠脊髓中催产素诱导的抗伤害感受。此外，鞘内注射μ受体拮抗剂β-芬太尼和κ受体拮抗剂去甲二氢吗啡酮可减弱催产素的抗伤害感受作用，但δ受体拮抗剂纳曲吲哚则无此作用，说明μ受体和κ受体而非δ受体参与了炎症大鼠脊髓中催产素诱导的抗伤害感受。此外，单独鞘内注射阿托西班可使炎症大鼠产生痛觉过敏，表明内源性催产素参与了炎症大鼠脊髓中伤害性信息的传递和调节。本研究表明，外源性和内源性催产素在炎症大鼠脊髓中均表现出抗伤害感受作用，且μ受体和κ受体参与了催产素诱导的抗伤害感受。
