Is there a relationship between 5-HT1B receptors and the mechanisms of action of antidepressant drugs in the learned helplessness paradigm in rats?

The present study was undertaken to investigate, in the learned helplessness paradigm, (1) the effects of CGS 12066B, a selective 5-HT1B receptor agonist administered alone, and (2) the effects of CGS612066B co-asministered with tricyclics (clomipramine, imipramine) or 5-HT re-uptake blockers (citalopram, fluvoxamine). The results showed that (1) the selective 5-HT1B agonist failed to reverse the escape deficit, and (2) in the drug interaction studies, CGS 12066B did not modify the ability of tricyclics to reverse the escape deficit. The 5-HT1B agonist, however, did significantly reduce the ability of 5-HT re-uptake blockers to reverse the escape deficit. The e result suggest that modulation of 5-HT1B sites might modify the enhancement of 5-HT neurotransmission by antidepressants, particularly 5-HT re-uptake blockers.