Barakol, a natural anxiolytic, inhibits striatal dopamine release but off uptake in vitro

The present study investigated the effects of barakol on the in vitro release of endogenous and radiolabelled dopamine from rat striatal slices in comparison with the dopamine receptor agonists, quinelorane dihydrochloride (1 microM) and pergolide methanesulfonate (100 microM), and the dopamine receptor antagonist, S(-)-eticlopride hydrochloride (10 microM) using a semi-superfusion method and high-performance liquid chromatography with electrochemical detector measurement of endogenous dopamine. Barakol (1, 10 and 100 microM) reduced K(+)-stimulated endogenous dopamine release as did the dopamine D2 receptor agonists but had no effect on [3H]dopamine release. The inhibition of barakol (10 microM) on K(+)-stimulated endogenous dopamine release was antagonised by a dopamine D2 receptor antagonist, eticlopride. Barakol (0.1 nM-10 microM) had no effect on [3H]dopamine uptake except at the highest concentration (100 microM) when inhibition was observed. The results indicate that barakol might act as a dopamine agonist to inhibit endogenous dopamine release without a change in dopamine uptake.