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Published on: January 10, 2011
Voltage- and Ca2+-activated potassium channels in Ca2+ store control Ca2+ release
Masayuki Yamashita1, Miho Sugioka, Yoichi Ogawa
1Department of Physiology I, Nara Medical University, Kashihara, Japan. yama@naramed-u.ac.jp
Calcium (Ca2+) release from stores is quantal. Big or maxi-K (BK) channels in the Ca2+ store regulate this release by closing as Ca2+ efflux decreases K+ influx, allowing for repetitive Ca2+ release.
Area of Science:
- Cellular Biology
- Ion Channel Function
- Calcium Signaling
Background:
- Calcium (Ca2+) release from intracellular stores exhibits quantal behavior, terminating after rapid efflux.
- The mechanism attenuating Ca2+ efflux, despite decreased luminal Ca2+, remains unclear.
Purpose of the Study:
- To elucidate the molecular mechanism controlling the quantal nature of Ca2+ release from stores.
- To identify the specific ion channels involved in regulating Ca2+ store release dynamics.
Main Methods:
- Utilized patch-clamp recordings from the nuclear envelope to study ion channel activity.
- Employed organelle-specific voltage-sensitive dyes (DiOC5(3)) to monitor luminal potential changes.
- Investigated the role of potassium channels in Ca2+ store release.
Main Results:
- Identified big or maxi-K (BK)-type potassium channels in the Ca2+ store as regulators of Ca2+ release.
- Demonstrated that BK channel closure, triggered by Ca2+ efflux, leads to lumen-negative potentials and suppresses further Ca2+ release.
- Showed that Ca2+ pumps and K+ influx regenerate BK channel activity, enabling repetitive Ca2+ release and bistable luminal potential oscillations.
Conclusions:
- Ca2+ efflux-induced closure of store BK channels attenuates Ca2+ release by reducing counter-influx of K+.
- BK channels act as a crucial feedback mechanism controlling the quantal release of Ca2+ from intracellular stores.
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