用β-内啡肽进行预处理可促进由δ-阿片受体反义寡脱氧核苷酸引起的δ-阿片受体介导的抗伤害感受的减弱。

Pretreatment with beta-endorphin facilitates the attenuation of delta-opioid receptor-mediated antinociception caused by delta-opioid receptor antisense oligodeoxynucleotide.

作者信息

Tseng L F, Narita M, Kampine J P

机构信息

Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.

出版信息

Eur J Pharmacol. 1995 Dec 12;287(2):169-72. doi: 10.1016/0014-2999(95)00587-0.

DOI:10.1016/0014-2999(95)00587-0

PMID:8749031

Abstract

Intracerebroventricular (i.c.v.) pretreatment of male ICR mice with beta-endorphin (0.6 nmol) or intrathecal (i.t.) pretreatment with antisense oligodeoxynucleotide to delta-opioid receptor mRNA (163 pmol) alone given 24 h earlier did not have any effect on i.t. administered delta-opioid receptor agonist [D-Ala2]deltorphin II (6.4 nmol)-induced antinociception. However, a concomitant i.c.v. pretreatments with beta-endorphin (0.08-0.6 nmol) and i.t. pretreatment with delta-opioid receptor antisense oligodeoxynucleotide (163 pmol) for 24 h dose-dependently attenuated i.t. challenged [D-Ala2]deltorphin II-induced antinociception. A concomitant i.c.v. pretreatment with mu-opioid receptor agonist [D-Ala2,N MePhe4,Gly(ol)5]enkephalin (DAMGO) or kappa-opioid receptor agonist U50,488H and i.t. pretreatment with delta-opioid receptor antisense oligodeoxynucleotide for 24 h did not affect i.t. challenged [D-Ala2]deltorphin II-induced antinociception. beta-Endorphin given supraspinally has been documented to release [Met5]enkephalin acting on delta-opioid receptors in the spinal cord. Our results indicate that supraspinal pretreatment with beta-endorphin selectively causes a loss of spinal delta-opioid receptor-mediated antinociception in mice receiving delta-opioid receptor antisense oligodeoxynucleotide.

摘要

雄性ICR小鼠在24小时前单独进行脑室内（i.c.v.）注射β-内啡肽（0.6 nmol）预处理或鞘内（i.t.）注射δ-阿片受体mRNA反义寡脱氧核苷酸（163 pmol）预处理，对鞘内注射δ-阿片受体激动剂[D-Ala2]强啡肽II（6.4 nmol）诱导的镇痛作用没有任何影响。然而，β-内啡肽（0.08 - 0.6 nmol）的脑室内联合预处理和δ-阿片受体反义寡脱氧核苷酸（163 pmol）的鞘内预处理24小时，可剂量依赖性地减弱鞘内注射[D-Ala2]强啡肽II诱导的镇痛作用。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的脑室内联合预处理与δ-阿片受体反义寡脱氧核苷酸的鞘内预处理24小时，并不影响鞘内注射[D-Ala2]强啡肽II诱导的镇痛作用。已证明脊髓上给予β-内啡肽可释放作用于脊髓中δ-阿片受体的[Met5]脑啡肽。我们的结果表明，在接受δ-阿片受体反义寡脱氧核苷酸的小鼠中，β-内啡肽的脊髓上预处理选择性地导致脊髓δ-阿片受体介导的镇痛作用丧失。