Differential mechanisms mediating beta-endorphin- and morphine-induced analgesia in mice.
Differential mechanisms mediating beta-endorphin- and morphine-induced analgesia in mice.
复制标题
介导小鼠β-内啡肽和吗啡诱导镇痛的不同机制。
DOI：
10.1016/0014-2999(89)90633-x
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发表时间：
1989
影响因子：
5
通讯作者：
Tseng,LL
中科院分区：
文献类型：
--
作者：
Suh,HH;Fujimoto,JM;Tseng,LL
鞘内（i.t.）育亨宾、美西麦角和纳洛酮以及脑室内（i.c.v.）给予纳洛酮对抑制β-内啡肽和吗啡诱导的甩尾和热板反应的影响。在雄性 ICR 小鼠中进行了研究。皮下注射育亨宾（1.5 和 15 μg）和美西麦角（1.5 和 15 μg）。拮抗吗啡诱导的甩尾反应的抑制，但不是静脉注射β-内啡肽。另一方面，纳洛酮 (20 ng) 注射到体内。拮抗对静脉注射引起的甩尾反应的抑制给予β-内啡肽但不给予吗啡。育亨宾和美西麦角给予它。不拮抗吗啡引起的热板反应的抑制，纳洛酮也没有拮抗吗啡引起的热板反应的抑制。对抗 i.c.v. β-内啡肽诱导的热板反应抑制。纳洛酮静脉注射在拮抗吗啡诱导的甩尾和热板反应抑制方面，比注射β-内啡肽诱导的抑制更有效。纳洛酮的剂量（0.1 和 1 μg）可有效逆转对静脉注射的甩尾反应的抑制。吗啡不能有效逆转静脉注射。 β-内啡肽诱导的甩尾反应抑制。我们的结果表明，β-内啡肽和吗啡通过刺激不同类型的阿片受体（β-内啡肽的 ε- 和吗啡的 μ-）产生镇痛作用，并激活单独的下行疼痛调节控制系统。 β-内啡肽刺激的脊髓上ε系统是通过脊髓阿片受体的激活介导的，而吗啡刺激的脊髓上μ系统是通过脊髓α2-受体和血清素受体的激活介导的，以产生镇痛。
Effects of yohimbine, methysergide and naloxone given intrathecally (i.t.) and naloxone given intracerebroventricularly (i.c.v.) on inhibition of the tail-flick and hot-plate response induced by β-endorphin and morphine given i.c.v. were studied in male ICR mice. Yohimbine (1.5 and 15 μg) and methysergide (1.5 and 15 μg) injected i.t. antagonized inhibition of the tail-flick response induced by morphine but not β-endorphin administered i.c.v. On the other hand, naloxone (20 ng) injected i.t. antagonized inhibition of the tail-flick response induced by i.c.v. administered β-endorphin but not morphine. Yohimbine and methysergide given i.t. did not antagonize inhibition of the hot-plate response induced by morphine nor did naloxone given i.t. antagonized i.c.v. β-endorphin-induced inhibition of the hot-plate response. Naloxone given i.c.v. was more effective in antagonizing morphine-induced inhibition of the tail-flick and hot-plate response than inhibition induced by β-endorphin given i.c.v. Naloxone at doses (0.1 and 1 μg) which effectively reversed inhibition of the tail-flick response to i.c.v. morphine was not effective in reversing the i.c.v. β-endorphin-induced inhibition of the tail-flick response. Our results indicate that β-endorphin and morphine produce analgesia by stimulating separate types of opioid receptors, ϵ- for β-endorphin and μ- for morphine, and activate separate descending pain modulatory control systems. The supraspinal ϵ system stimulated by β-endorphin is mediated by activation of spinal opioid receptors whereas the supraspinal μ system stimulated by morphine is mediated by activation of spinalα2-adreceptors and serotonin receptors for the production of analgesia.