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J Biol Chem, Vol. 274, Issue 52, 36957-36962, December 24, 1999

Low Cytoplasmic [Ca²⁺] Activates I_CRAC Independently of Global Ca²⁺ Store Depletion in RBL-1 Cells^*

Elmar Krause, Andreas Schmid, Antonio González, and Irene Schulz

From the 2. Physiologisches Institut, Universität des Saarlandes, D-66421 Homburg/Saar, Germany

Release of Ca²⁺ from inositol (1,4,5)-trisphosphate-sensitive Ca²⁺ stores causes "capacitative calcium entry," which is mediated by the so-called "Ca²⁺ release-activated Ca²⁺ current" (I_CRAC) in RBL-1 cells. Refilling of the Ca²⁺ stores or high cytoplasmic [Ca²⁺] ([Ca²⁺]_cyt) inactivate I_CRAC. Here we address the question if also [Ca²⁺]_cyt lower than the resting [Ca²⁺]_cyt influences store-operated channels. We therefore combined patch clamp and mag fura-2 fluorescence methods to determine simultaneously both I_CRAC and [Ca²⁺] within Ca²⁺ stores of RBL-1 cells ([Ca²⁺]_store). We found that low [Ca²⁺]_cyt in the range of 30-50 nM activates I_CRAC and Ca²⁺ influx spontaneously and independently of global Ca²⁺ store depletion, while elevation of [Ca²⁺]_cyt to the resting [Ca²⁺]_cyt (100 nM) resulted in store dependence of I_CRAC activation. We conclude that spontaneous activation of I_CRAC by low [Ca²⁺]_cyt could serve as a feedback mechanism keeping the resting [Ca²⁺]_cyt constant.

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^* The costs of publication of this article were defrayed in part by the payment of page charges. The 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: 2. Physiologisches Institut, Universität des Saarlandes, D-66421 Homburg/Saar, Germany. Tel.: 49-6841-16-6450; Fax: 49-6841-16-6655; E-mail: schulz@med-ph.uni-sb.de.

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Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.

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