Key result
Coexpression of the beta1 subunit increased burst duration approximately 20-fold and gap duration 3-fold, resulting in a 10-fold increase in open probability in the absence of intracellular Ca2+.
The major effects of the beta1 subunit on BK channel gating are independent of intracellular Ca2+, suggesting it mainly alters the energy barriers of Ca2+-independent transitions.
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BK channel beta1 effects occur without Ca2+; extends gating models but leaves open cardiovascular translation.
Coexpression of the beta(1) subunit with the alpha subunit (mSlo) of BK channels increases the apparent Ca(2+) sensitivity of the channel. This study investigates whether the mechanism underlying the increased Ca(2+) sensitivity requires Ca(2+), by comparing the gating in 0 Ca(2+)(i) of BK channels composed of alpha subunits to those composed of alpha+beta(1) subunits. The beta(1) subunit increased burst duration approximately 20-fold and the duration of gaps between bursts approximately 3-fold, giving an approximately 10-fold increase in open probability (P(o)) in 0 Ca(2+)(i). The effect of the beta(1) subunit on increasing burst duration was little changed over a wide range of P(o) achieved by varying either Ca(2+)(i) or depolarization. The effect of the beta(1) subunit on increasing the durations of the gaps between bursts in 0 Ca(2+)(i) was preserved over a range of voltage, but was switched off as Ca(2+)(i) was increased into the activation range. The Ca(2+)-independent, beta(1) subunit-induced increase in burst duration accounted for 80% of the leftward shift in the P(o) vs. Ca(2+)(i) curve that reflects the increased Ca(2+) sensitivity induced by the beta(1) subunit. The Ca(2+)-dependent effect of the beta(1) subunit on the gaps between bursts accounted for the remaining 20% of the leftward shift. Our observation that the major effects of the beta(1) subunit are independent of Ca(2+)(i) suggests that the beta(1) subunit mainly alters the energy barriers of Ca(2+)-independent transitions. The changes in gating induced by the beta(1) subunit differ from those induced by depolarization, as increasing P(o) by depolarization or by the beta(1) subunit gave different gating kinetics. The complex gating kinetics for both alpha and alpha+beta(1) channels in 0 Ca(2+)(i) arise from transitions among two to three open and three to five closed states and are inconsistent with Monod-Wyman-Changeux type models, which predict gating among only one open and one closed state in 0 Ca(2+)(i).
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Nimigean et al. (2000) studied this question. Coexpression of beta1 subunit with alpha subunit (mSlo) of BK channels vs. alpha subunit alone was evaluated on Gating kinetics (burst duration, gap duration, open probability) in 0 Ca2+i. Coexpression of the beta1 subunit increased burst duration approximately 20-fold and gap duration 3-fold, resulting in a 10-fold increase in open probability in the absence of intracellular Ca2+.
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