Participation of an α2-mediated mechanism in the production of forced swimming-stress induced analgesia in mice

Abstract

In mice, both swimming-stress induced analgesia (SW-SIA) and Clonidine (CLO) analgesia were dose dependently antagonized by yohimbine, an α2-adrenoceptor antagonist, but not by naloxone, an opioid μ-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 α2-adrenergic-dependent mechanism, for their production. © 1991, The Pharmaceutical Society of Japan. All rights reserved.