Calcitonin, a peptide hormone expressed in C-cells of the thyreoid gland, as well as capsaicin, isolated from chili, both, modify intracellular signalling in nociceptive neurones. The pathways triggered by the activation of either of these receptors results in a modulation of the intracellular calcium ([Ca2+]i) concentration. While the regulation of [Ca2+]i depends on many factors, voltage activated calcium channels (VACCs) are a major gate for the calcium entry into neurones. Here we describe the changes of voltage gated calcium channel currents (ICa(V)) induced by calcitonin and/or capsaicin. Currents were recorded using adequate solutions and voltage protocols with the whole cell patch-clamp technique. When the channels were opened by a depolarisation to 0mV, both substances reduce the peak ICa(V) (calcitonin (10nM): 29.3±3.9%; capsaicin (0.5μM): 41.1±7.7%). While the effect of calcitonin was voltage dependent, capsaicin shifted the largest current to the more hyperpolarizing range (peak current from -10 to -20mV). A subsequent co-application of either of the two substances (with a pre-application of either 3min or 60min) results in an additive reduction of the currents, and prevents the capsaicin-induced shift of the current-voltage relation. Therefore, we hypothesize, that the activation of either of the two receptors reduces ICa(V) by different cellular binding sites of the channel protein triggering channel opening. These findings may be useful to understand cellular mechanisms of pain modulation and might help to find better treatments for neuropathic pain.
|Number of pages||6|
|Journal||Brain Research Bulletin|
|Publication status||Published - 25 Apr 2011|
- Neuropathic pain
- Voltage activated calcium channel currents
ASJC Scopus subject areas