Calcitonin, a hormone released from the C-cells of the thyroid gland, tightly regulates the calcium concentrations in blood. Calcium is an important second messenger for intracellular mechanisms and therefore also influences pain signalling. Recently it has been shown, that dorsal root ganglion (DRG) neurones smaller than 20mm coexpress calcitonin and pain (TRPV1) receptors. Therefore we analysed the effect of calcitonin (from salmon) on calcium entry through voltage gated calcium channel currents (VACCCs) in isolated DRG neurones of 21 day old "Wistar" rats. Patch clamp technique experiments revealed a difference in response to calcitonin concerning peak- and sustained currents of VACCCs. The application of 10 nM calcitonin resulted in a reduction of the VACCC of ~30% (peak current) to ~60% (sustained current). Furthermore, we analysed whether a pretreament with calcitonin modifies the capsaicin induced reduction of VACCCs (see Hagenacker et al., 2005; IC₅₀ for VACCCs was ~0.36mM). Indeed, a pre-treatment with 10nM calcitonin for 1h abolishes the capsaicin induced reduction of the VACCC nearly completely. An inadequate high concentration of capsaicin (10mM) was needed to reduce the current about 40%. We conclude, that the calcium regulating effect of calcitonin also affects VACCCs of DRG neurones. This modulation might be of importance in regard to analgetic effects of calcitonin.