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Chunk #28 — RESULTS — Decay of STOCs is determined by the kinetics of BK channels

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Spatial organization of RYRs and BK channels underlying the activation of STOCs by Ca(2+) sparks in airway myocytes.
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Our previous study in amphibian gastric stomach cells indicated that BK channel kinetics plays a key role in determining the decay of STOCs (ZhuGe et al., 2002) because [Ca2+] is very low during the STOC decay. If this is also the case in ASM, we would expect that (a) the decay of STOCs would follow a single exponential function with a time constant close to the mean open time of BK channels and (b) the decay of STOCs would be independent of their own amplitude and Ca2+ spark amplitude. We tested these possibilities by first examining STOCs and their corresponding Ca2+ sparks. STOC decay can be fitted with a single exponential with a τ of 29 ± 3 ms (n = 45), which is close to the mean open time of BK channels in smooth muscle (Singer and Walsh, 1987; Tanaka et al., 1997; Harper et al., 2001; Lu et al., 2008; Yang et al., 2009). Moreover, no correlation between signal mass and STOC decay was present (r = 0.0091, P = 0.9588, n = 35; Fig. 2 A), nor was STOC amplitude and STOC decay correlated (r = 0.3227, P = 0.0587, n = 35; Fig. 2 A).