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α2介导机制在小鼠强迫游泳应激诱导镇痛产生中的作用。

Participation of an alpha 2-mediated mechanism in the production of forced swimming-stress induced analgesia in mice.

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

J Pharmacobiodyn. 1991 Jun;14(6):357-61. doi: 10.1248/bpb1978.14.357.

Abstract

In mice, both swimming-stress induced analgesia (SW-SIA) and clonidine (CLO) analgesia were dose dependently antagonized by yohimbine, an alpha 2-adrenoceptor antagonist, but not by naloxone, an opioid mu-antagonist. SW-SIA was potentiated by subanalgesic dose of CLO, and CLO analgesia was enhanced by SW-SIA. Animals tolerant to CLO analgesia were tolerant to SW-SIA, in contrast, CLO analgesia was potentiated in SW-SIA tolerant mice. Thus, SW-SIA and CLO analgesia partially share a common alpha 2-adrenergic-dependent mechanism, for their production.

摘要

在小鼠中,游泳应激诱导的镇痛(SW-SIA)和可乐定(CLO)镇痛均呈剂量依赖性地被α2肾上腺素能受体拮抗剂育亨宾拮抗,但不被阿片μ受体拮抗剂纳洛酮拮抗。亚镇痛剂量的CLO可增强SW-SIA,而SW-SIA可增强CLO镇痛。对CLO镇痛产生耐受的动物对SW-SIA也产生耐受,相反,在对SW-SIA产生耐受的小鼠中CLO镇痛增强。因此,SW-SIA和CLO镇痛在产生过程中部分共享一种常见的α2肾上腺素能依赖性机制。

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