Calcitonin is used for the treatment of bone pain. While its actions in osteohomeostasis are well known, it remains unclear how it modulates pain signals. Recently we have demonstrated for capsaicin that it modulates nociceptive signals by differential reduction of voltage activated calcium channel currents (VACCs) in small nociceptive neurones. Since the calcitonin receptor and TRPV-1 are co-expressed in these neurones we tested whether calcitonin modulates VACCS itself and whether it interferes with the capsaicin action on VACCS.

VACCs were recorded from neurones cultured from 21 day old "wistar" rats, using the whole-cell patch-clamp technique. The application of 10nM calcitonin reduces VACC by 25.67% (±1.78%), while that current was 78.67% (±4.59%) reduced with 0.5mM capsaicin. Pre-application of 10nM calcitonin, followed by an application of 0.5mM capsaicin reduced the current first by 19.42% (±8.24%) and than by another 20.92% (±12.68%). This is an indication that possibly cross-links in the molecular pathways between these mediating analgetic effects exists. Pre-incubation with 10nM calcitonin for 60min resulted in the same reduction of the current, indicating that acute interactions occure, while analgetic long-term effects were mediated by other pathways, e.g. affecting the bone homeostasis.