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Voltage‐ and Ca 2+ ‐activated potassium channels in Ca 2+ store control Ca 2+ release
Author(s) -
Yamashita Masayuki,
Sugioka Miho,
Ogawa Yoichi
Publication year - 2006
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/j.1742-4658.2006.05365.x
Subject(s) - chemistry , potassium , bk channel , biophysics , potassium channel , depolarization , calcium , membrane potential , efflux , sodium , biochemistry , biology , organic chemistry
Ca 2+ release from Ca 2+ stores is a ‘quantal’ process; it terminates after a rapid release of stored Ca 2+ . To explain the quantal nature, it has been supposed that a decrease in luminal Ca 2+ acts as a ‘brake’ on store release. However, the mechanism for the attenuation of Ca 2+ efflux remains unknown. We show that Ca 2+ release is controlled by voltage‐ and Ca 2+ ‐activated potassium channels in the Ca 2+ store. The potassium channel was identified as the big or maxi‐K (BK)‐type, and was activated by positive shifts in luminal potential and luminal Ca 2+ increases, as revealed by patch‐clamp recordings from an exposed nuclear envelope. The blockage or closure of the store BK channel due to Ca 2+ efflux developed lumen‐negative potentials, as revealed with an organelle‐specific voltage‐sensitive dye [DiOC 5 (3); 3,3’‐dipentyloxacarbocyanine iodide], and suppressed Ca 2+ release. The store BK channels are reactivated by Ca 2+ uptake by Ca 2+ pumps regeneratively with K + entry to allow repetitive Ca 2+ release. Indeed, the luminal potential oscillated bistably by ∼45 mV in amplitude. Our study suggests that Ca 2+ efflux‐induced store BK channel closures attenuate Ca 2+ release with decreases in counter‐influx of K + .