Antinociception Induced by Amitriptyline and Imipramine Is Mediated by α2A-Adrenoceptors

The Japanese Journal of Pharmacology

Nicoletta Galeotti¹  Alessandro Bartolini¹  Carla Ghelardini¹ 

[1] Department of Preclinical and Clinical Pharmacology,University of Florence,Viale G.Pieraccini,6,I-50139 Florence,Italy

关键词: Analgesia;    Amitriptyline;    Imipramine;    α2A-Adrenoceptor;    Tricyclic antidepressant;   

DOI  :  10.1254/jjp.82.130

学科分类：药理学

来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society

【 摘 要 】

References(42)Cited-By(39)The involvement of α2-adrenoceptors in the antinociception induced by the tricyclic antidepressants amitriptyline and imipramine was investigated in mice by using the hot-plate and abdominal constriction tests.The antinociception produced by amitriptyline(15mg/kg, i.p.) and imipramine(15mg/kg, i.p.) was prevented by reserpine(2mg/kg, i.p.) and yohimbine(3-10mg/kg, i.p.) but not by naloxone(1mg/kg, i.p.), atropine(5mg/kg, i.p.), CGP 35348(100mg/kg, i.p.) and prazosin(1mg/kg, i.p.).On the basis of the above data, it can be postulated that amitriptyline and imipramine exerted their antinociceptive effect by activation of α2-adrenoceptors.Administration of the α2A-adrenoceptor antagonist BRL 44408(1mg/kg, i.p.) prevented amitriptyline and imipramine antinociception, whereas the α2B/C-adrenoceptor antagonist ARC 239(10mg/kg, i.p.) was ineffective.These data indicate that the enhancement of the pain threshold produced by amitriptyline and imipramine is mediated by activation of α2A-adrenoceptors.Neither tricyclic antidepressants nor the antagonists used impaired mouse performance evaluated by the rota-rod and hole-board tests.

【 授权许可】

Unknown