Raffa R B, Martinez R P
Drug Discovery Research, R. W. Johnson Pharmaceutical Research Institute, Spring House, PA 19477-0776.
Eur J Pharmacol. 1992 May 14;215(2-3):357-8. doi: 10.1016/0014-2999(92)90060-h.
Pretreatment (18 h) of mice with a single s.c. injection of LiCl (10 mmol/kg) reduced the antinociceptive action of centrally administered (i.c.v.) morphine in the tail-flick test (ED50 = 7.7 micrograms) compared to vehicle-treated controls (ED50 = 1.8 micrograms). The coadministration of inositol-1,4,5-trisphosphate (IP3; 20 micrograms) with morphine restored the morphine-induced antinociception (ED50 = 2.4 micrograms) in LiCl-pretreated mice to control levels. These finding implicate a LiCl-sensitive (possibly phosphoinositide) second messenger pathway in the mediation of morphine-induced analgesia.
与赋形剂处理的对照组（半数有效量=1.8微克）相比，单次皮下注射氯化锂（10毫摩尔/千克）对小鼠进行预处理（18小时），可降低在甩尾试验中脑室内注射吗啡的镇痛作用（半数有效量=7.7微克）。在氯化锂预处理的小鼠中，将肌醇-1,4,5-三磷酸（IP3；20微克）与吗啡共同给药，可使吗啡诱导的镇痛作用（半数有效量=2.4微克）恢复至对照水平。这些发现表明，在吗啡诱导的镇痛作用介导过程中，存在一条对氯化锂敏感（可能是磷酸肌醇）的第二信使途径。
