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Additive inhibitory effects of calcitonin and capsaicin on voltage activated calcium channel currents in nociceptive neurones of rat.

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.

journal_name

Brain Res Bull

journal_title

Brain research bulletin

authors

Hagenacker T,Ledwig D,Büsselberg D

doi

10.1016/j.brainresbull.2011.02.006

subject

Has Abstract

pub_date

2011-04-25 00:00:00

pages

75-80

issue

1-2

eissn

0361-9230

issn

1873-2747

pii

S0361-9230(11)00070-0

journal_volume

85

pub_type

杂志文章

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