Myricetin, is a naturally occurring flavonoid found in grapes, berries, fruits, vegetables, herbs, as well as other plants. Beside its anti-oxidant, anti-neoplastic and anti-inflammatory effects it has analgetic properties in experimental pain syndromes. Although its analgetic effect has been well studied, up to now the molecular mechanisms remain unclear. Acute i.p-injections of myricetin in rodents with neuropathic pain syndromes lead to a dose-dependent pain-reduction in behavioral studys. Because of its acute analgetic effect voltage activated channels has been suggested to be involved in this process. In this study voltage activated calcium and potassium channel currents were isolated in cultured dorsal root ganglion (DRG) neurones of rats using the whole cell patch-clamp method and Ba²⁺ as charge carrier. While voltage activated potassium channel currents (VAPC) were dose-dependently reduced by myricetin voltage activated calcium channel currents (VACC) were modulated differentially. Application of minor concentrations (0.1mM-5mM) of myricetin reduces the current in a range of 10.62%-56.3% while depolarizing the membrane to 0mV. Concentrations of myrecitin > 10mM lead to an increase of the current up to 20.47% using 100mM of myricetin. For it is known, that myricetin-effects were partially mediated by p38-cascades, a p38-inhibitor (SB 220025) was pre-applied (10mM for 30min) on the cell. After myrecitin-application the reduction of VACC currents in minor concentrations was slightly enhanced, while the increase of the current after application of myricetin in concentrations >10mM was diminished. Therefore we propose different intracellular pathways for both effects of myricetin on VACCs, with a partial involvement of the p38-signal cascade. These findings may be of relevance for the development of flavonoid-based anti-nociceptive and anti-neoplastic drugs.