Narita M, Tseng L F
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226, USA.
Eur J Pharmacol. 1995 Sep 15;284(1-2):185-9. doi: 10.1016/0014-2999(95)00414-g.
Intrathecal (i.t.) pretreatment of male ICR mice with antisense oligodeoxynucleotide to delta-opioid receptor mRNA once a day for 1-3 days caused a time-dependent attenuation of i.t. administered [D-Ala2]deltorphin II-induced antinociception as measured by the tail-flick test. The attenuation of the antinociception induced by i.t. administered [D-Ala2]deltorphin II, a delta-opioid receptor agonist, was enhanced by i.t. pretreatment for 1 day with [D-Ala2]deltorphin II, but not [D-Ala2,N MePhe4,Gly(ol)5]enkephalin (DAMGO), a mu-opioid receptor agonist, or U50,488H, a kappa-opioid receptor agonist, given together with antisense oligodeoxynucleotide to delta-opioid receptor mRNA. The present results indicate that stimulation of spinal delta-opioid receptors by i.t. injection of [D-Ala2]deltorphin II selectively causes a loss of delta-opioid receptor-mediated antinociception in mice pretreated with antisense oligodeoxynucleotide to delta-opioid receptor mRNA.
对雄性ICR小鼠鞘内（i.t.）注射δ-阿片受体mRNA反义寡脱氧核苷酸，每天一次，持续1 - 3天，通过甩尾试验测量发现，这会导致鞘内注射[D-Ala2]强啡肽II诱导的镇痛作用出现时间依赖性减弱。鞘内注射δ-阿片受体激动剂[D-Ala2]强啡肽II诱导的镇痛作用减弱，在与δ-阿片受体mRNA反义寡脱氧核苷酸一起进行1天的鞘内预处理时，会因同时给予[D-Ala2]强啡肽II而增强，但μ-阿片受体激动剂[D-Ala2，N-MePhe4，Gly(ol)5]脑啡肽（DAMGO）或κ-阿片受体激动剂U50,488H则不会增强。目前的结果表明，鞘内注射[D-Ala2]强啡肽II刺激脊髓δ-阿片受体，会选择性地导致在用δ-阿片受体mRNA反义寡脱氧核苷酸预处理的小鼠中，δ-阿片受体介导的镇痛作用丧失。
