Yohimbine's anxiogenic action: Evidence for noradrenergic and dopaminergic sites

Abstract Yohimbine (2.5 or 4 mg/kg) reduced the percentage of open arm entries and the percentage of time spent on the open arms displayed by rats on an elevated plus-maze indicating anxiogenic activity. These effects were reversed by the α 2 -adrenoceptor agonist clonidine (0.01 mg/kg) and by the dopamine receptor agonist apomorphine (0.57 mg/kg). The following failed to reverse the effects of yohimbine: the selective α 2 -adrenoceptor agonists, guanfacine (0.25 and 1 mg/kg), B-HT920 (0.025 and 0.1 mg/kg), B-HT933 (1 and 10 mg/kg); the β-blocker propanolol (2.5 and 10 mg/kg); the α 1 -adrenoceptor agonist phenylephrine; the D 1 agonist SK&F 38393 (5 and 10 mg/kg) and the D 2 agonist LY 171555 (0.5 and 1 mg/kg). Therefore, it is unlikely that activity at only the α 1 , α 2 , β, D 1 or D 2 sites can entirely account for the anxiogenic actions of yohimbine in the elevated plus-maze. Evidence that clonidine affects the dopaminergic system and that apomorphine affects the noradrenergic system suggests that yohimbine may produce its anxiogenic response by activity on both the noradrenergic and dopaminergic systems.