Jg. Mcgeown et al., THE TEMPORAL PROFILE OF CALCIUM TRANSIENTS IN VOLTAGE-CLAMPED GASTRICMYOCYTES FROM BUFO-MARINUS, Journal of physiology, 497(2), 1996, pp. 321-336
1. Decay in intracellular calcium concentration ([Ca2+](i)) was record
ed following step depolarizations in voltage clamped gastric myocytes
from Bufo marinus. 2. Depolarizations (300 ms) to +10 mV were followed
by three phases of [Ca2+](i) decay with repolarization to both -110 a
nd -50 mV. The decline was initially rapid (mean fractional decay rate
= 81 +/- 11% s(-1) at -110 mV), then slowed (decay rate = 14 +/- 2% s
(-1)) and finally accelerated again (decay rate = 24 +/- 3% s(-1); n =
19). 3. The initial phase of rapid decay became shorter as the length
of the depolarizing pulse increased but was unaffected by changes in
pulse voltage. 4. The delayed acceleration in [Ca2+](i) decay was no l
onger seen when the duration of the depolarizing pulses was reduced to
100 ms, but was clearly evident following 500 ms pulses. This phase w
as abolished when the depolarizing voltage was altered to minimize the
rise in [Ca2+](i). 5. Ryanodine and caffeine had no effect on the tem
poral profile of [Ca2+](i) decay. 6. Removal of extracellular Na+ decr
eased the decay rate during all three phases at -110 mV, but this effe
ct was particularly marked for the initial rapid phase of decay, the r
ate of which was reduced by 75%. A delayed increase in decay rate was
still seen. 7. Inhibition of mitochondrial Ca2+ uptake with cyanide, c
arbonyl cyanide p-trifluoromethoxyphenylhydrazone or Ruthenium Red had
no effect on the initial rate of [Ca2+](i) decay but blocked the dela
yed acceleration.