Journal
JAPANESE JOURNAL OF PHARMACOLOGY
Volume 82, Issue 2, Pages 130-137Publisher
JAPANESE PHARMACOLOGICAL SOC
DOI: 10.1254/jjp.82.130
Keywords
analgesia; amitriptyline; imipramine; alpha(2A)-adrenoceptor; tricyclic antidepressant
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The involvement of alpha(2)-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 (15 mg/kg, i.p.) and imipramine (15 mg/kg, i.p.) was prevented by reserpine (2 mg/kg, i.p.) and yohimbine (3 - 10 mg/kg, i.p.) but not by naloxone (1 mg/kg, i.p.), atropine (5 mg/kg, i.p.), CGP 35348 (100 mg/kg, i.p.) and prazosin (1 mg/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 alpha(2)-adrenoceptors. Administration of the alpha(2A)-adrenoceptor antagonist BRL 44408 (1 mg/kg, i.p,) prevented amitriptyline and imipramine antinociception, whereas the alpha(2B/C)-adrenoceptor antagonist ARC239 (10 mg/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 alpha(2A)-adrenoceptors. Neither tricyclic antidepressants nor the antagonists used impaired mouse performance evaluated by the rota-rod and hole-board tests.
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