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D-青霉胺2-D-青霉胺5-脑啡肽或D-丙氨酸2-N-甲基苯丙氨酸4-甘氨醇-脑啡肽对脊髓中β-氯诺昔明的保护作用,对小鼠脑室内注射β-内啡肽诱导的抗伤害感受的影响。

The effects of protection by D-Pen2-D-Pen5-enkephalin or D-Ala2-NMePhe4-Gly-ol-enkephalin against beta-chlornaltrexamine in the spinal cord on the antinociception induced by beta-endorphin administered intracerebroventricularly in the mouse.

作者信息

Suh H W, Lim J S, Song D K, Kim Y H, Tseng L F

机构信息

Department of Pharmacology, College of Medicine, Hallym University, Chunchon, Kangwon-Do, Korea.

出版信息

Neuropeptides. 1994 Aug;27(2):143-9. doi: 10.1016/0143-4179(94)90055-8.

DOI:10.1016/0143-4179(94)90055-8
PMID:7991069
Abstract

Chlornaltrexamine (beta-CNA, 0.5 micrograms) alone or beta-CNA plus either mu-agonist, D-Ala2-NMePhe4-Gly-ol-enkephalin (DAMGO, 500 ng) or delta-agonist, D-Pen2-D-Pen5-enkephalin (DPDPE, 10 micrograms) was injected intrathecally (i.t.) to protect mu- or delta-opioid receptors, respectively, for 24 h in male ICR mice. The antinociception was assessed by the tail-flick and hot-plate test. DPDPE or DAMGO injected i.t. increased inhibition of the tail-flick and hot-plate response in a dose-dependent manner. The dose-response curve for tail-flick and hot-plate response induced by DPDPE or DAMGO in i.t. saline-treated group significantly shifted to the right in i.t. beta-CNA alone treated group but returned to the control level in the group treated with i.t. beta-CNA coadministered with DPDPE or DAMGO, respectively. The effects of protection of mu- and delta-opioid receptor in the spinal cord on inhibition of the tail-flick and hot-plate response induced by beta-endorphin and morphine administered intracerebroventricularly (i.c.v.) were then studied. Intrathecal pretreatment with beta-CNA or beta-CNA coadministered with DAMGO attenuated inhibition of the tail-flick response induced by beta-endorphin administered i.c.v. However, i.t. treatment with beta-CNA coadministered with DPDPE did not affect inhibition of the tail-flick response induced by beta-endorphin administered i.c.v. Intrathecal pretreatment with beta-CNA or beta-CNA coadministered with either DPDPE or DAMGO did not alter inhibition of the hot-plate response induced by beta-endorphin administered i.c.v.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

将氯诺他明(β-CNA,0.5微克)单独或与μ-激动剂D-Ala2-NMePhe4-Gly-ol-脑啡肽(DAMGO,500纳克)或δ-激动剂D-Pen2-D-Pen5-脑啡肽(DPDPE,10微克)联合鞘内注射(i.t.),分别在雄性ICR小鼠中保护μ-或δ-阿片受体24小时。通过甩尾试验和热板试验评估镇痛作用。鞘内注射DPDPE或DAMGO以剂量依赖性方式增加对甩尾和热板反应的抑制。在鞘内盐水处理组中,由DPDPE或DAMGO诱导的甩尾和热板反应的剂量反应曲线在单独鞘内注射β-CNA的组中显著右移,但在分别与DPDPE或DAMGO联合鞘内注射β-CNA的组中恢复到对照水平。然后研究了脊髓中μ-和δ-阿片受体的保护对脑室内(i.c.v.)注射β-内啡肽和吗啡诱导的甩尾和热板反应抑制的影响。鞘内用β-CNA或与DAMGO联合鞘内注射β-CNA预处理减弱了脑室内注射β-内啡肽诱导的甩尾反应抑制。然而,与DPDPE联合鞘内注射β-CNA处理不影响脑室内注射β-内啡肽诱导的甩尾反应抑制。鞘内用β-CNA或与DPDPE或DAMGO联合鞘内注射β-CNA预处理不改变脑室内注射β-内啡肽诱导的热板反应抑制。(摘要截短于250字)

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