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Modulation of intracellular calcium influences capsaicin-induced currents of TRPV-1and voltage-activated channel currents in nociceptive neurones

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Modulation of intracellular calcium ([Ca2+]i) has a major impact on processing of nociceptive signals. While activation of the transient receptor potential vanilloid-1 (TRPV-1) receptor/channel complex increases [Ca2+]i by Ca2+ entry from the extracellular space, as well as by Ca2+ release from intracellular stores, the Ca2+ entry through voltage-activated calcium channels (VACCs) is modulated simultaneously. To clarify the relations between [Ca2+]i and the activation of TRPV-1 receptor and VACC currents [ITRPV-1 and ICa(V)], we performed voltage clamp experiments using Ba2+ as well as Ca2+ as a charge carrier. The TRPV-1 receptor was activated by the application of 0.5 M capsaicin, and the currents through TRPV-1 and VACC [ITRPV-1 and ICa(V)] were measured either when Ca2+ release from intracellular stores was pharmacologically promoted or prevented. With Ba2+ as the divalent charge carrier, capsaicin (0.5 M) reduced ICa(V) (elicited by a depolarization to 0 mV) to 52.7 ± 4.5% of baseline, and the elicited current through the TRPV-1 receptor/channel complex was 6.6 ± 0.9% [relative to peak ICa(V)]. These currents were significantly different when Ca2+ was used as charge carrier: the ICa(V) reductions were decreased to 17.8 ± 5.9% of baseline, while the ITRPV-1 was as high as 57.1 ± 9.1% of ICa(V). Increases of [Ca2+]i by releasing Ca2+ from intracellular stores (using caffeine, 10 mM) before the application of capsaicin increased the ITRPV-1 (14.1 ± 7%), while the ICa(V) was decreased to 51.6 ± 4.9% compared with control. A preexperimental partial reduction of the Ca2+ release from the stores by dantrolene (5 M) resulted in less pronounced effects [24.5 ± 8.8%, relative to peak ICa(V)] for ITRPV-1, and a reduction to 35.4 ± 3% of baseline for ICa(V) after capsaicin application.
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Keywords: TRPV-1; capsaicin; intracellular calcium; nociception; voltage-activated calcium channel currents

Document Type: Research Article

Affiliations: Institut für Physiologie, Universitätsklinikum Essen, Essen, Germany

Publication date: December 1, 2007

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