ABSTRACT
Kavain and dihydromethysticin were shown to decrease the amplitude of field potential changes in guinea pig hippocampus slices extracellularly treated with the serotonin agonist ipsapirone (Bayer AG, Leverkusen, Ger many), an experimental antidepressant and anxiolytic agent. The effect was dose dependent and significant in a range of concentrations corresponding to previously estimated steadγ-state/therapeutic concentrations of kava pγrones (50-150 µMol/L). After 45 min the effect was completely reversible. The results of the experiment indicate that dihydromethysticin and kavain may elicit anxiolytic effects through modulation of serotonin1A receptors (Walden et al., 1997). Serdarevic et al. (2001) examined the acute effects of a kava extract (LI 158, 30% kavalactones) on the neurotransmitter levels of mice. Administered at doses of 250 and 500 mg/kg p.o., only the higher dose produced a significant decrease in dopamine levels and although it ap peared to cause an insignificant decrease in serotonin levels, levels of the se rotonin metabolite 5-hydroxyindolacetic acid (5HIAA) levels were signifi cantly enhanced. Norepinephrine (NE) levels remained unchanged, as did levels of homovanillic acid (HVA), and 3,4-dihydroxyphenyl-αcetic acid (DOPAC). By comparison, an extract of St. John’s wort (LI 160) had no ef fect on NE levels, caused a significant increase in brain levels of HVA, DOPAC, and 5HIAA, and also slightly decreased dopamine levels, again, only from the higher dose. These results indicate that compared to the St. John’s wort extract, the kava extract is only a weak antidepressant and/or modifier of brain neurotransmitter concentrations in the mouse.
