Chung K M, Kim Y H, Song D K, Huh S O, Suh H W
Department of Pharmacology, Institute of Natural Medicine, College of Medicine, Hallym University, Chunchon, Kangwon Do, South Korea.
Neuropeptides. 1999 Dec;33(6):534-41. doi: 10.1054/npep.1999.0775.
Our previous studies have demonstrated that supraspinal GABAergic receptors are differentially involved in the antinociception induced by morphine and beta-endorphin given intracerebroventricularly (i.c.v.) in the tail-flick and hot-plate tests. These two models employed a phasic, thermal nociceptive stimulus. The present study was designed to examine the possible involvement of supraspinal GABAergic receptors in opioid-induced antinociception in the formalin test. Morphine (1 microg) and beta-endorphin (1 microg) given i.c.v. displayed the almost complete inhibitory effects against the hyperalgesic response in both phases. Muscimol (75-100 ng) and baclofen (5-10 ng) injected i.c.v. produced the hypoalgesic response in the both phases. The hypoalgesic response induced by muscimol and baclofen observed during the second phase was more pronounced than that observed during the second phase. Baclofen (2.5 ng), at the dose which did not affect the hyperalgesic response, resulted in a significant reversal of the i.c.v. administered beta-endorphin-induced hypoalgesic response observed during the second, but not the first, phase. However, the hypoalgesic response induced by i.c.v. administered morphine was not changed by the same dose of muscimol or baclofen injected i.c.v. Our results indicate that, at the supraspinal level, GABA(B)receptors appear to be involved in the modulation of antinociception induced by supraspinally administered beta-endorphin, but not morphine, in the formalin test model.
我们之前的研究表明，在甩尾和热板试验中，脊髓上的GABA能受体以不同方式参与脑室内（i.c.v.）注射吗啡和β-内啡肽所诱导的抗伤害感受。这两种模型采用的是阶段性热伤害性刺激。本研究旨在检测脊髓上的GABA能受体在福尔马林试验中阿片类药物诱导的抗伤害感受中可能发挥的作用。脑室内注射吗啡（1微克）和β-内啡肽（1微克）在两个阶段均对痛觉过敏反应表现出几乎完全的抑制作用。脑室内注射蝇蕈醇（75 - 100纳克）和巴氯芬（5 - 10纳克）在两个阶段均产生痛觉减退反应。在第二阶段观察到的由蝇蕈醇和巴氯芬诱导的痛觉减退反应比第一阶段更明显。在不影响痛觉过敏反应的剂量下，巴氯芬（2.5纳克）能显著逆转在第二阶段（而非第一阶段）观察到的脑室内注射β-内啡肽所诱导的痛觉减退反应。然而，脑室内注射吗啡所诱导的痛觉减退反应不会因相同剂量的脑室内注射蝇蕈醇或巴氯芬而改变。我们的结果表明，在脊髓上水平，在福尔马林试验模型中，GABA(B)受体似乎参与脊髓上注射β-内啡肽（而非吗啡）所诱导的抗伤害感受的调节。
