Further Evidence for the Participation of an α₂-Adrenoceptor Mediated Mechanism in the Production of Forced Swimming-Stress Induced Analgesia in Mice

Abstract

Subanalgesic dose, 0.01 to 0.25 mg/kg, of clonidine (CLO), an α₂-adrenoceptor agonist, potentiated forced swimming (SW) stress induced analgesia (SIA) and suppressed psychological (PSY)-SIA in a dose dependent manner but did not affect foot-shock (FS)-SIA. Daily exposure to each stress rapidly developed tolerance, and the development was suppressed by daily concomitant subanalgesic dose of CLO in SW-SIA but not in FS- and PSY-SIA. Meanwhile, SW-stress, applied after injection of CLO, 1 mg/kg, potentiated the analgesic effect of CLO and suppressed the development of tolerance to the effect. On the other hand, FS- and PSY-stress did not affect CLO analgesia and failed to block the tolerance development. These results provide further evidence that α₂-adrenergic mechanism is involved in the production of SW-SIA.