Depletion of calcium from the sarcoplasmic reticulum during calcium release in frog skeletal muscle.

Schneider, Martin F.; Simon, Bruce J.; Szücs, G.

doi:10.1113/jphysiol.1987.sp016775

Cited by 80 publications

(109 citation statements)

References 19 publications

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“…The average delay was somewhat briefer than in sparks, perhaps because the action potential synchronizes not just the beginning but also the termination of sparks (17). Unlike skraps, cell-wide depletion did not visibly recover by 600 ms, which agrees with refilling times estimated by global photometry (18). The faster recovery of single skraps suggests that local depletion is replenished by diffusion from neighboring SR regions.…”

Section: Simultaneoussupporting

confidence: 74%

Depletion “skraps” and dynamic buffering inside the cellular calcium store

Launikonis

Zhou²,

Royer³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

154

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Ca 2؉ signals, produced by Ca 2؉ release from cellular stores, switch metabolic responses inside cells. In muscle, Ca 2؉ sparks locally exhibit the rapid start and termination of the cell-wide signal. By imaging Ca 2؉ inside the store using shifted excitation and emission ratioing of fluorescence, a surprising observation was made: Depletion during sparks or voltage-induced cell-wide release occurs too late, continuing to progress even after the Ca 2؉ release channels have closed. This finding indicates that Ca 2؉ is released from a ''proximate'' compartment functionally in between store lumen and cytosol. The presence of a proximate compartment also explains a paradoxical surge in intrastore Ca 2؉ , which was recorded upon stimulation of prolonged, cell-wide Ca 2؉ release. An intrastore surge upon induction of Ca 2؉ release was first reported in subcellular store fractions, where its source was traced to the store buffer, calsequestrin. The present results update the evolving concept, largely due to N. Ikemoto and C. Kang, of calsequestrin as a dynamic store. Given the strategic location and reduction of dimensionality of Ca 2؉ -adsorbing linear polymers of calsequestrin, they could deliver Ca 2؉ to the open release channels more efficiently than the luminal store solution, thus constituting the proximate compartment. When store depletion becomes widespread, the polymers would collapse to increase store [Ca 2؉ ] and sustain the concentration gradient that drives release flux.calcium signaling ͉ calcium sparks ͉ excitation-contraction coupling ͉ sarcoplasmic reticulum ͉ skeletal muscle R apid changes in intracellular cytosolic [Ca 2ϩ ] are required for signaling functions in many cell types (1). These changes are achieved via Ca 2ϩ release through channels, ryanodine receptors (RyRs), which must open and close quickly. To increase its speed, gating of RyRs relies on effects of the permeant ion, including channel opening by elevated cytosolic [Ca 2ϩ ] (2). In muscle, the desirable fast kinetic features are already present in its elementary signaling events, Ca 2ϩ sparks (3), which involve the nearly simultaneous opening (4) of a number of channels (5), followed by their synchronized closing (4). Thus, this gating does not follow the usual Markovian rules for channels that evolve independently but requires timekeeping and synchronization (6). In cardiac muscle, depletion of sarcoplasmic reticulum (SR) Ca 2ϩ is the likely timer of channel closing, and the substantial depletion that follows the cardiac beat (7) was imaged as ''blinks'' associated with Ca 2ϩ sparks (8). The sensor that translates depletion into channel closing appears to be the main intra-SR buffer, calsequestrin (CSQ) (9).By contrast, in skeletal muscle, depletion associated with a twitch is only 8-15% (10). This low rate of depletion reflects a SR with larger terminal cisternae containing higher concentrations of a CSQ of greater binding capacity, thus constituting a much greater calcium reservoir. Despite the greater store, sparks of skeletal mus...

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Section: Simultaneoussupporting

confidence: 74%

Depletion “skraps” and dynamic buffering inside the cellular calcium store

Launikonis

Zhou²,

Royer³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

154

View full text Add to dashboard Cite

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“…In our hands, one stimulation per minute is considered as optimal. Results of experiments by Schneider et al (1987) suggested that the SR could be depleted of Ca 2+ after a conditioning TEST pulse when [EGTA] in the internal solution was only 0.1 mM. Garcia et al (1989) also observed a substantial depletion of Ca 2+ in the SR by repetitive stimulation at 0.03 Hz when [EGTA] in the internal solution was 1 mM.…”

Section: Effects Of the Interventions On I~ And I Vmentioning

confidence: 76%

Factors affecting the appearance of the hump charge movement component in frog cut twitch fibers.

Hui

1991

The Journal of General Physiology

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Charge movement was measured in frog cut twitch fibers with the double Vaseline gap technique. Five manipulations listed below were applied to investigate their effects on the hump component (Iv) in the ON segments of TEST minus CONTROL current traces. When external CI-was replaced by MeSO~ to eliminate CI current, I v peaked earlier due to a few millivolts shift of the voltage dependence of I, kinetics in the negative direction. The Q-V plots in the TEA.CI and TEA.MeSO~ solutions were well fitted by a sum of two Boltzmann distribution functions. The more steeply voltage-dependent component (Q,) had a F ~ 6 mV more negative in the TEA.MeSO s solution than in the TEA.CI solution. These voltage shifts were partially reversible. When creatine phosphate in the end pool solution was removed, the I v hump disappeared slowly over the course of 20-30 min, partly due to a suppression of Qv' The hump reappeared when creatine phosphate was restored. When 0.2-1.0 mM Cd 2+ was added to the center pool solution to block inward Ca current, the I v hump became less prominent due to a prolongation in the time course of I v but not to a suppression of Qv" When the holding potential was changed from -90 to -120 mV, the amplitude of Ia was increased, thereby obscuring the I v hump. Finally, when a cut fiber was stimulated repetitively, I, lost its hump appearance because its time course was prolonged. In an extreme case, a 5-rain resting interval was insufficient for a complete recovery of the waveform. In general, a stimulation rate of once per minute had a negligible effect on the shape of I v. Of the five manipulations, MeSO~ has the least perturbation on the appearance of I v and is potentially a better substitute for C1-than SO~-in eliminating CI current if the appearance of the I v hump is to be preserved.

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“…Such changes in [Ca]; may be too small to fully explain the frequency-dependent depression of AH by Ca induced inactivation of Ca release channels. Furthermore, the recovery from the inactiva tion of Ca release channels is more rapid (within 1 sec) than refilling depleted SR (over 10 sec) in the skeletal muscle (20,21). We, however, can not rule out the possible in activation processes of intracellular Ca release during repetitive stimulation.…”

Section: Discussionmentioning

confidence: 97%

Ryanodine suppresses the frequency-dependent component of the spike after-hyperpolarization in the rat superior cervical ganglion.

Kawai

Watanabe

1991

Jpn.J.Pharmacol

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ABSTRACT-The spike after-hyperpolarization (AH), which is linked to the Ca-acti vated K conductance system, in the rat superior cervical ganglion was examined by means of intracellular recording. The AH was shortened during repetitive stimulation of the cell at 1 Hz and reached a steady state within 10 sec. These changes in the AH disappeared after a part of the AH was depressed by 5 ,u M ryanodine. The steady state of AHs was dependent on the frequency of stimulation ranging from 0.005 Hz and 2 Hz; half depression was observed at 0.53 Hz. Half recovery time from the de pression induced by conditioning stimuli at 2 Hz was approximately 14 sec. Caffeine (1 mM) or TEA (3 mM) enlarged the AH at low stimulation frequencies. Caffeine slight ly shifted the frequency depressing the AH toward high frequencies, and TEA did not cause significant changes. These results suggest that the repetitive firing of cells de creases the intracellular Ca release by contributing to the generation of the AH, rather than by accelerating the loading of Ca to its storage sites.

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Depletion of calcium from the sarcoplasmic reticulum during calcium release in frog skeletal muscle.

Cited by 80 publications

References 19 publications

Depletion “skraps” and dynamic buffering inside the cellular calcium store

Depletion “skraps” and dynamic buffering inside the cellular calcium store

Factors affecting the appearance of the hump charge movement component in frog cut twitch fibers.

Ryanodine suppresses the frequency-dependent component of the spike after-hyperpolarization in the rat superior cervical ganglion.

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