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阿片受体烷基化后的恢复:β-氯代纳曲酮处理小鼠的社会冲突镇痛和脑内[³H]埃托啡结合

Recovery from opioid receptor alkylation: social conflict analgesia and brain [3H]etorphine binding in beta-chlornaltrexamine-treated mice.

作者信息

Lazega D, Frischknecht H R, Waser P G, Siegfried B

机构信息

Institute of Pharmacology, University of Zürich, Switzerland.

出版信息

Eur J Pharmacol. 1988 Oct 18;155(3):333-7. doi: 10.1016/0014-2999(88)90525-0.

DOI:10.1016/0014-2999(88)90525-0
PMID:2853070
Abstract

The effects of beta-chlornaltrexamine (CNA, 5 mg/kg s.c.) on social conflict analgesia and brain opioid binding were investigated in mice at different times after the administration of the alkylating antagonist. The specific binding of [3H]etorphine to high-affinity binding sites and the stress-induced analgesia of attacked mice (50 bites) were prevented for 6 h after CNA administration. Stress-mediated inhibition of pain fully recovered within 3 days after CNA treatment. Brain opioid binding was still reduced to 45% at this time and reached control values 9 days after treatment.

摘要

研究了β-氯诺美沙明(CNA,5毫克/千克,皮下注射)对给予烷化拮抗剂后不同时间小鼠的社会冲突镇痛和脑阿片类物质结合的影响。给予CNA后6小时,[3H]埃托啡与高亲和力结合位点的特异性结合以及受攻击小鼠(50次咬伤)的应激诱导镇痛被阻断。CNA治疗后3天内,应激介导的疼痛抑制完全恢复。此时脑阿片类物质结合仍降至45%,治疗9天后达到对照值。

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