Br-16a does not interfere with alpha - 2 noradrenergic and dopamine postsynaptic receptor functioning.

BR-16A is a herbal preparation with several putative psychotropic effects. Recent work has suggested that it facilities certain aspects of cognition and that it ameliorates ECT-induced amnesia in animal models. The present study sought to assess whether it affects noradrenergic and dopaminergic functioning in the central nervous system. Adult male Sprague-Dawley rats received BR-16A (200mg/kg) or vehicle for one month. The animals were subsequently challenged with clonidine (100 mg/kg I.P.), apomorphine (2mg/kg I.P.), or saline in a factorial design, and motility of the animals was immediately thereafter assessed using a small open field. BR-16A neither attenuated clonidine induced alpha-2 noradrenergic receptor-mediated hypomotility nor accentuated apomorphine-induced dopamine postsynaptic receptor-mediated hypermotility, suggesting that it does not interfere with alpha-2 noradrenergic and dopamine postsynaptic receptor functioning.