Nociceptor activation results in the generation of action potentials, which are transmitted to the CNS giving the sensation of pain. The TRPV1 receptor is one of the most important pain receptors. We analysed effects of capsaicin, an agonist of the TRPV1 receptor, on specific types of voltage activated calcium (VAC), potassium (VAP) as well as on TTX resistant and total voltage activated sodium channel (VASC) currents. Isolated neurones from dorsal root ganglion of 3-4 days old Wistar rats, were used for whole cell patch clamp recordings. Voltage gated calcium, potassium or sodium channels were isolated and different concentrations of capsaicin were applied. Only in small DRG neurones (<30mm) subtypes of voltage gated calcium channel currents were differentially sensitive to capsaicin, most likely due to the expression of the TRPV1 receptor. Overall, VAC channels were reduced by 50% at a concentration of 0.36mM, but different channel subtypes were differentially modulated. Concentrations of up to 20mM of capsaicin had only minor effects on potassium channel currents (~10% reduction at 20mM). The total VASC were reduced by capsaicin in low concentrations (0.5mM, 40–50% reduction), and the effect is even more pronounced in TTX-resistant sodium currents (0.1mM, ~30% reduction). We conclude, that the different effects of capsaicin on voltage activated channels were responsible for the complex pain modulation at the spinal level.