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Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada 89557-0046
Localized Ca2+ transients resulting from inositol
trisphosphate (IP3)-dependent Ca2+ release
couple to spontaneous transient outward currents (STOCs) in murine
colonic myocytes. Confocal microscopy and whole cell patch-clamp
techniques were used to investigate coupling between localized
Ca2+ transients and STOCs. Colonic myocytes were loaded
with fluo 3. Reduction in external Ca2+
([Ca2+]o) reduced localized Ca2+
transients but increased STOC amplitude and frequency. Simultaneous recordings of Ca2+ transients and STOCs showed increased
coupling strength between Ca2+ transients and STOCs when
[Ca2+]o was reduced. Gd3+ (10 µM) did not affect Ca2+ transients but increased STOC
amplitude and frequency. Similarly, an inhibitor of Ca2+
influx,
1-2-(4-methoxyphenyl)-2-[3-(4-methoxyphenyl)propoxy]ethyl-1H-imidazole (SKF-96365), increased STOC amplitude and frequency. A protein kinase C
(PKC) inhibitor, GF-109203X, also increased the amplitude and frequency
of STOCs but had no effect on Ca2+ transients. Phorbol
12-myristate 13-acetate (1 µM) reduced STOC amplitude and frequency
but did not affect Ca2+ transients. 4
-Phorbol (1 µM)
had no effect on STOCs or Ca2+ transients. Single channel
studies indicated that large-conductance Ca2+-activated
K+ (BK) channels were inhibited by a
Ca2+-dependent PKC. In summary 1)
Ca2+ release from IP3 receptor-operated stores
activates Ca2+-activated K+ channels;
2) Ca2+ influx through nonselective cation
channels facilitates activation of PKC; and 3) PKC reduces
the Ca2+ sensitivity of BK channels, reducing the coupling
strength between localized Ca2+ transients and BK channels.
calcium puffs; spontaneous transient outward current; gastrointestinal motility; inositol 1,4,5-trisphosphate; sarcoplasmic reticulum
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