These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Additive inhibitory effects of calcitonin and capsaicin on voltage activated calcium channel currents in nociceptive neurones of rat.
    Author: Hagenacker T, Ledwig D, Büsselberg D.
    Journal: Brain Res Bull; 2011 Apr 25; 85(1-2):75-80. PubMed ID: 21335070.
    Abstract:
    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 ([Ca(2+)](i)) concentration. While the regulation of [Ca(2+)](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 (I(Ca(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 0 mV, both substances reduce the peak I(Ca(V)) (calcitonin (10nM): 29.3 ± 3.9%; capsaicin (0.5 μM): 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 -20 mV). A subsequent co-application of either of the two substances (with a pre-application of either 3 min or 60 min) 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 I(Ca(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.
    [Abstract] [Full Text] [Related] [New Search]