Suh H W, Song D K, Kim Y H
Department of Pharmacology, College of Medicine, Hallym University, Chunchon, Kangwon-Do, South Korea.
Neuropeptides. 1997 Aug;31(4):339-44. doi: 10.1016/s0143-4179(97)90069-x.
A previous study reported that beta-endorphin and morphine administered supraspinally produce antinociception by activating different descending pain inhibitory systems. The present study was designed to investigate the blocking effects of A1 or A2 adenosine receptors in the spinal cord on antinociception induced by supraspinally administered mu- and epsilon-opioid receptor agonists. The effects of 1,3-dipropyl-8-(2-amino-4-chloro-phenyl)-xanthine (PACPX; an A1 adenosine receptor antagonist) or 3,7-dimethyl-1-propargylxanthine (DMPX; an A2 adenosine receptor antagonist) on the antinociception induced by morphine (a mu-opioid receptor agonist) or beta-endorphin (an epsilon-opioid receptor agonist) administered intracerebroventricularly (i.c.v.) were studied. The antinociception was assayed by the tail-flick test. DMPX at doses of 1-40 micrograms (which administered intrathecally alone did not affect the latencies of tail-flick thresholds), attenuated dose-dependently the inhibition of the tail-flick response induced by i.c.v. administered morphine (0.5 microgram) or beta-endorphin (1 microgram). PACPX at doses of 1-40 micrograms (which administered intrathecally alone did not affect the latencies of tail-flick thresholds), attenuated dose-dependently the inhibition of the tail-flick response induced by i.c.v. administered beta-endorphin but not morphine. These results suggest that A2 but not A1 adenosine receptors in the spinal cord may be involved in the antinociception induced by supraspinally administered morphine, while the antinociception induced by supraspinally administered beta-endorphin appears to be mediated by spinal A1 and A2 adenosine receptors. These results support the hypothesis that morphine and beta-endorphin administered supraspinally produce antinociception by different neuronal mechanisms.
先前的一项研究报告称，脑内注射β-内啡肽和吗啡通过激活不同的下行性疼痛抑制系统产生抗伤害感受作用。本研究旨在探讨脊髓中A1或A2腺苷受体阻断对脑内注射μ-和ε-阿片受体激动剂诱导的抗伤害感受的影响。研究了1,3-二丙基-8-(2-氨基-4-氯苯基)黄嘌呤（PACPX；一种A1腺苷受体拮抗剂）或3,7-二甲基-1-丙炔基黄嘌呤（DMPX；一种A2腺苷受体拮抗剂）对脑室内（i.c.v.）注射吗啡（一种μ-阿片受体激动剂）或β-内啡肽（一种ε-阿片受体激动剂）诱导的抗伤害感受的影响。通过甩尾试验测定抗伤害感受。剂量为1-40微克的DMPX（单独鞘内注射不影响甩尾阈值潜伏期），剂量依赖性地减弱了i.c.v.注射吗啡（0.5微克）或β-内啡肽（1微克）诱导的甩尾反应抑制。剂量为1-40微克的PACPX（单独鞘内注射不影响甩尾阈值潜伏期），剂量依赖性地减弱了i.c.v.注射β-内啡肽而非吗啡诱导的甩尾反应抑制。这些结果表明，脊髓中的A2而非A1腺苷受体可能参与脑内注射吗啡诱导的抗伤害感受，而脑内注射β-内啡肽诱导的抗伤害感受似乎由脊髓A1和A2腺苷受体介导。这些结果支持以下假说：脑内注射吗啡和β-内啡肽通过不同的神经元机制产生抗伤害感受作用。
