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通过苯二氮䓬受体介导机制,心理应激对吗啡镇痛耐受性发展的阻断作用。

Blockade of the development of analgesic tolerance to morphine by psychological stress through benzodiazepine receptor mediated mechanism.

作者信息

Tokuyama S, Takahashi M, Kaneto H

机构信息

Department of Pharmacology, Faculty of Pharmaceutical Sciences, Nagasaki University, Japan.

出版信息

Jpn J Pharmacol. 1989 Nov;51(3):425-7. doi: 10.1254/jjp.51.425.

DOI:10.1254/jjp.51.425
PMID:2560093
Abstract

beta-Carboline-3-carboxylic acid ethyl ester (beta-CCE) dose-dependently potentiated psychological-stress induced analgesia (PSY-SIA), and the effect was reversed by diazepam. Concurrent exposure to PSY stress or concomitant treatment with beta-CCE blocked the development of analgesic tolerance to morphine; the effect of PSY stress was antagonized by diazepam, and that of beta-CCE was reversed by Ro 15-1788. These results suggest that psychological factors which are mediated through benzodiazepine receptors are involved in the mechanism for blocking the development of analgesic tolerance to morphine by PSY stress.

摘要

β-咔啉-3-羧酸乙酯(β-CCE)能剂量依赖性地增强心理应激诱导的镇痛作用(PSY-SIA),且该作用可被地西泮逆转。同时暴露于PSY应激或与β-CCE同时给药可阻断对吗啡镇痛耐受性的形成;PSY应激的作用可被地西泮拮抗,而β-CCE的作用可被Ro 15-1788逆转。这些结果表明,通过苯二氮䓬受体介导的心理因素参与了PSY应激阻断对吗啡镇痛耐受性形成的机制。

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