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J. Biol. Chem., Vol. 280, Issue 8, 7022-7029, February 25, 2005

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Voltage-dependent Changes of TRPV6-mediated Ca²⁺ Currents^*

Matthias Bödding

From the Experimentelle und Klinische Pharmakologie und Toxikologie, Universität des Saarlandes, D-66421 Homburg, Germany

The physiological role and activation mechanism for most proteins of the transient receptor potential (TRP) family are unknown. This is also the case for the highly Ca²⁺ selective transient receptor potential vanilloid type 6 (TRPV6) channel. Patch clamp experiments were performed on transiently transfected human embryonic kidney (HEK) cells to address this issue. Currents were recorded under various conditions of intracellular Ca²⁺ buffering and monitored at the same voltage throughout. No TRPV6-mediated Ca²⁺ entry was detected under in vivo Ca²⁺ buffering conditions at a slightly negative holding potential; however, moderate depolarization resulted in current activation. Very similar results were obtained with different Ca²⁺ chelators, either EGTA or BAPTA dialyzing the cell. TRPV6 channel activity showed a negative correlation with the intracellular free Ca²⁺ concentration ([Ca²⁺]_i) and was modulated by the membrane potential: Hyperpolarization decreases and depolarization increases TRPV6-mediated currents. Monovalent ions permeated TRPV6 channels in the absence of extracellular divalent cations. These currents were resistant to changes in the holding potential while the negative correlation to the [Ca²⁺]_i was conserved, indicating that the voltage-dependent current changes depend on blocking and unblocking the charge carrier Ca²⁺ within the pore. In summary, these results suggest that the voltage dependence of TRPV6-mediated Ca²⁺ influx is of physiological importance since it occurs at cytosolic Ca²⁺ buffering and takes place within a physiologically relevant membrane potential range.

Received for publication, September 7, 2004 , and in revised form, December 2, 2004.

^* The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed. Tel.: 49-6841-1626242; Fax: 49-6841-1626402; E-mail: matthias.boedding{at}uniklinik-saarland.de.

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