The correlation between the increase in slow outward current and in contraction induced by caffeine, ryanodine, and rapid cooling in voltage-clamped frog muscle fibers

1991 ◽  
Vol 69 (6) ◽  
pp. 859-864 ◽  
Author(s):  
Mohammad Nasri-Sebdani ◽  
Flavien Traoré ◽  
Aklesso Mouzou ◽  
Christian Cognard ◽  
Daniel Potreau ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Muscle Fibers ◽  
Outward Current ◽  
Frog Muscle ◽  
Rapid Cooling ◽  
Key Words Skeletal Muscle ◽  
Parallel Increase ◽  
The One ◽  
Sarcoplasmic Reticulum Calcium

The effects of caffeine, ryanodine, and rapid cooling were tested on the depolarization-induced contraction and the apamin-insensitive slow outward current (Iso) of voltage-clamped (double mannitol gap) single frog muscle fibers. Subthreshold caffeine concentrations (0.5–2 mM) induced a monotonic increase in contractile and Iso amplitude. Whatever the concentration, the increase in contraction was roughly twice the one in current. Similar results were obtained upon rapid cooling (20–4 °C) in the presence of 0.5 mM caffeine. In the absence of external Na+ (choline-substituted) 10−5 M ryanodine induced a delayed increase (≈30 min) in contraction and in current, shortly before the development of a drastic and irreversible contracture. Here again, the increase in contraction was twice that in current. In the presence of 5 mM tetraethylammonium (TEA) and (or) 25 nM charybdotoxin, 2 mM caffeine still induced a strong facilitating effect on contraction but the parallel increase in current was strongly reduced. The linear relationship between the increase in current and contractile amplitude has a slope ≈0.5 (whatever the drug used to increase contractility); it is ≈0.1 in the presence of TEA and (or) charybdotoxin. In conclusion, provided the changes in contractile amplitude are caused by parallel changes in depolarization-induced sarcoplasmic reticulum Ca2+ release, about 50% of the apamin-insensitive Iso is controlled by internal Ca2+ release. The main part of this current corresponds to the TEA- and charybdotoxin-sensitive component of Iso.Key words: skeletal muscle, voltage clamp, Ca2+-dependent K+ current, sarcoplasmic reticulum calcium release, caffeine, ryanodine, charybdotoxin.

scholarly journals A slow component of intramembranous charge movement during sarcoplasmic reticulum calcium release in frog cut muscle fibers.

1996 ◽  
Vol 107 (1) ◽  
pp. 79-101 ◽  
Author(s):  
P C Pape ◽  
D S Jong ◽  
W K Chandler
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Rana Temporaria ◽  
Slow Component ◽  
Muscle Fibers ◽  
Charge Movement ◽  
Small Current ◽  
Sarcoplasmic Reticulum Calcium ◽  
A New Species ◽  
Peak Value

Cut muscle fibers from Rana temporaria were mounted in a double Vaseline-gap chamber and equilibrated with an end-pool solution that contained 20 mM EGTA and 1.76 mM Ca (sarcomere length, 3.3-3.8 microns; temperature, 14-16 degrees C). Sarcoplasmic reticulum (SR) Ca release, delta[CaT], was estimated from changes in myoplasmic pH (Pape, P.C., D.-S. Jong, and W.K. Chandler. 1995. J. Gen. Physiol. 106:259-336). The maximal value of delta[CaT] obtained during a depleting depolarization was assumed to equal the SR Ca content before stimulation, [CaSR]R (expressed as myoplasmic concentration). After a depolarization to -55 to -40 mV in fibers with [CaSR]R = 1,000-3,000 microM, currents from intramembranous charge movement, Icm, showed an early I beta component. This was followed by an I gamma hump, which decayed within 50 ms to a small current that was maintained for as long as 500 ms. This slow current was probably a component of Icm because the amount of OFF charge, measured after depolarizations of different durations, increased according to the amount of ON charge. Icm was also measured after the SR had been depleted of most of its Ca, either by a depleting conditioning depolarization or by Ca removal from the end pools followed by a series of depleting depolarizations. The early I beta component was essentially unchanged by Ca depletion, the I gamma hump was increased (for [CaSR]R > 200 microM), the slow component was eliminated, and the total amount of OFF charge was essentially unchanged. These results suggest that the slow component of ON Icm is not movement of a new species of charge but is probably movement of Q gamma that is slowed by SR Ca release or some associated event such as the accompanying increase in myoplasmic free [Ca] that is expected to occur near the Ca release sites. The peak value of the apparent rate constant associated with this current, 2-4%/ms at pulse potentials between -48 and -40 mV, is decreased by half when [CaSR]R approximately equal to 500-1,000 microM, which gives a peak rate of SR Ca release of approximately 5-10 microM/ms.

scholarly journals Impaired Sarcoplasmic Reticulum Calcium Release In Skeletal Muscle Fibers From Myotubularin-Deficient Mice

2009 ◽  
Vol 96 (3) ◽  
pp. 10a ◽  
Author(s):  
Norbert Weiss ◽  
Lama Al-Qusairi ◽  
Celine Berbey ◽  
Bruno Allard ◽  
Jean Louis Mandel ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Muscle Fibers ◽  
Skeletal Muscle Fibers ◽  
Sarcoplasmic Reticulum Calcium ◽  
Deficient Mice

scholarly journals Calcium- and voltage-activated plateau currents of cardiac Purkinje fibers.

1987 ◽  
Vol 89 (6) ◽  
pp. 921-958 ◽  
Author(s):  
J L Kenyon ◽  
J L Sutko
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Intracellular Calcium ◽  
Potassium Current ◽  
Calcium Release ◽  
Outward Current ◽  
Calcium Transient ◽  
Chloride Ions ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
Sarcoplasmic Reticulum Calcium

We have used the two-microelectrode voltage-clamp technique to investigate the components of membrane current that contribute to the formation of the early part of the plateau phase of the action potential of calf cardiac Purkinje fibers. 3,4-Diaminopyridine (50 microM) reduced the net transient outward current elicited by depolarizations to potentials positive to -30 mV but had no consistent effect on contraction. We attribute this effect to the blockade of a voltage-activated transient potassium current component. Ryanodine (1 microM), an inhibitor of sarcoplasmic reticulum calcium release and intracellular calcium oscillations in Purkinje fibers (Sutko, J.L., and J.L. Kenyon. 1983. Journal of General Physiology. 82:385-404), had complex effects on membrane currents as it abolished phasic contractions. At early times during a depolarization (5-30 ms), ryanodine reduced the net outward current. We attribute this effect to the loss of a component of calcium-activated potassium current caused by the inhibition of sarcoplasmic reticulum calcium release and the intracellular calcium transient. At later times during a depolarization (50-200 ms), ryanodine increased the net outward current. This effect was not seen in low-sodium solutions and we could not observe a reversal potential over a voltage range of -100 to +75 mV. These data suggest that the effect of ryanodine on the late membrane current is attributable to the loss of sodium-calcium exchange current caused by the inhibition of sarcoplasmic reticulum calcium release and the intracellular calcium transient. Neither effect of ryanodine was dependent on chloride ions, which suggests that chloride ions do not carry the ryanodine-sensitive current components. Strontium (2.7 mM replacing calcium) and caffeine (10 mM), two other treatments that interfere with sarcoplasmic reticulum function, had effects in common with ryanodine. This supports the hypothesis that the effects of ryanodine may be attributed to the inhibition of sarcoplasmic reticulum calcium release.

Two sites of action for LCB29 (idrocilamide) in depressing mechanical tension of rat soleus muscle fibers?

1993 ◽  
Vol 71 (12) ◽  
pp. 889-895
Author(s):  
Aklesso Mouzou ◽  
Alexandre Bouron ◽  
Joel Guillemain ◽  
Daniel Guerrier ◽  
Guy Raymond
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Soleus Muscle ◽  
Calcium Release ◽  
Muscle Fibers ◽  
Voltage Sensor ◽  
Dependent Inactivation ◽  
Voltage Dependent ◽  
Rat Soleus Muscle ◽  
Sarcoplasmic Reticulum Calcium ◽  
Caffeine Contractures

The effects of 50 μM LCB29 (idrocilamide) were tested on depolarization-induced and caffeine contractures of rat soleus muscle fibers. When applied intracellularly by free diffusion in cut-end voltage-clamped fibers, LCB29 decreased tension amplitude by about 25%. The same amount of inhibition by LCB29 was observed on contractures induced by 6 mM caffeine. The drug did not affect the repriming of caffeine contractures, indicating that internal recycling of calcium was not affected. The voltage-dependent inactivation of tension was facilitated by external application of LCB29. This effect was calcium dependent, so that the greater the external calcium concentration, the greater the drug effectiveness. The spontaneous relaxation of K+ contractures was also accelerated by LCB29. It is concluded that LCB29 acts intracellularly by decreasing sarcoplasmic reticulum calcium release and externally by facilitating the voltage-dependent inactivation of the voltage sensor for excitation–contraction coupling.Key words: myorelaxants, skeletal muscle, sarcoplasmic reticulum calcium release, voltage sensor.

scholarly journals Flecainide Inhibits Cardiac Ryanodine Channels And Spontaneous Sarcoplasmic Reticulum Calcium Release In Casq2 Null Myocytes

2009 ◽  
Vol 96 (3) ◽  
pp. 11a
Author(s):  
Derek Laver ◽  
Nagesh Chopra ◽  
Bjorn C. Knollmann
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Sarcoplasmic Reticulum Calcium

scholarly journals Cardiac Sarcoplasmic Reticulum Calcium Release and Load Are Enhanced by Subcellular cAMP Elevations in PI3Kγ-Deficient Mice

2005 ◽  
Vol 96 (10) ◽  
pp. 1079-1086 ◽  
Author(s):  
Benoit-Gilles Kerfant ◽  
Dominica Gidrewicz ◽  
Hui Sun ◽  
Gavin Y. Oudit ◽  
Josef M. Penninger ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Sarcoplasmic Reticulum Calcium ◽  
Deficient Mice
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