Xu J Y, Tseng L F
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226.
Eur J Pharmacol. 1994 Sep 12;262(3):223-31. doi: 10.1016/0014-2999(94)90736-6.
(+)-cis-Dioxolane (0.5-2 micrograms), a muscarinic receptor agonist, given intracerebroventricularly (i.c.v.) produced a dose-dependent inhibition of the tail-flick response in male ICR mice. (+)-cis-Dioxolane given i.c.v. at a subanalgesic dose (0.25 micrograms), selectively potentiated the antinociceptive response induced by i.c.v. administered beta-endorphin, an epsilon-opioid receptor agonist, but not morphine or [D-Ala2,NMePhe4,Gly5-ol]enkephalin (DAMGO), mu-opioid receptor agonists, [D-Pen2,D-Pen5]enkephalin (DPDPE), a delta receptor agonist, or trans(+/-)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]- benzeneacetamide methane sulfonate (U50,488H), a kappa-opioid receptor agonist. The antinociceptive response induced by (+)-cis-dioxolane given i.c.v. was attenuated by i.c.v. treatment with N omega-nitro-L-arginine (1 microgram), hemoglobin (120 micrograms) or methylene blue (10 micrograms). The antinociception induced by carbachol given i.c.v. was also antagonized by the i.c.v. treatment with N omega-nitro-L-arginine (1 microgram). However, the same treatment with N omega-nitro-L-arginine, hemoglobin or methylene blue did not affect the beta-endorphin-induced antinociception. The potentiation of beta-endorphin-induced antinociception by (+)-cis-dioxolane was reversed by i.c.v. treatment with N omega-nitro-L-arginine (1 microgram), hemoglobin (120 micrograms) or methylene blue (10 micrograms). On the other hand, the antinociceptive response induced by (+)-cis-dioxolane (1 microgram) given i.c.v. was potentiated by i.c.v. administered L-arginine (20 micrograms) but not D-arginine (20 micrograms). Dibutyryl cyclic GMP at 0.5-2.0 micrograms given i.c.v. produced an antinociceptive response and at subanalgesic dose (0.1 microgram) potentiated i.c.v. beta-endorphin-induced antinociception.(ABSTRACT TRUNCATED AT 250 WORDS)
（+）-顺式二氧戊环（0.5 - 2微克），一种毒蕈碱受体激动剂，脑室内注射（i.c.v.）可对雄性ICR小鼠的甩尾反应产生剂量依赖性抑制。以亚镇痛剂量（0.25微克）脑室内注射（+）-顺式二氧戊环，可选择性增强脑室内注射的β-内啡肽（一种ε-阿片受体激动剂）诱导的镇痛反应，但对吗啡或[D-Ala2，NMePhe4，Gly5-ol]脑啡肽（DAMGO，μ-阿片受体激动剂）、[D-Pen2，D-Pen5]脑啡肽（DPDPE，δ受体激动剂）或反式（+/-）-3,4-二氯-N-甲基-N-[2-（1-吡咯烷基）环己基]苯乙酰胺甲磺酸盐（U50,488H，κ-阿片受体激动剂）诱导的镇痛反应无增强作用。脑室内注射（+）-顺式二氧戊环诱导的镇痛反应可被脑室内注射Nω-硝基-L-精氨酸（1微克）、血红蛋白（120微克）或亚甲蓝（10微克）减弱。脑室内注射卡巴胆碱诱导的镇痛作用也可被脑室内注射Nω-硝基-L-精氨酸（1微克）拮抗。然而，相同剂量的Nω-硝基-L-精氨酸、血红蛋白或亚甲蓝处理并不影响β-内啡肽诱导的镇痛作用。（+）-顺式二氧戊环对β-内啡肽诱导的镇痛作用的增强可被脑室内注射Nω-硝基-L-精氨酸（1微克）、血红蛋白（12�微克）或亚甲蓝（10微克）逆转。另一方面，脑室内注射（+）-顺式二氧戊环（1微克）诱导的镇痛反应可被脑室内注射L-精氨酸（20微克）增强，但D-精氨酸（20微克）无此作用。脑室内注射0.5 - 2.0微克的二丁酰环磷鸟苷可产生镇痛反应，以亚镇痛剂量（0.1微克）可增强脑室内注射β-内啡肽诱导的镇痛反应。（摘要截短于250字）
