scholarly journals THE RESTING MEMBRANE POTENTIAL AND CATION MOVEMENT IN FROG MUSCLE FIBERS AFTER EXPOSURE TO LITHIUM IONS

1967 ◽  
Vol 17 (6) ◽  
pp. 678-697 ◽  
Author(s):  
Ken'ichi YONEMURA ◽  
Masayasu SATO
Keyword(s):  
Membrane Potential ◽  
Muscle Fibers ◽  
Frog Muscle ◽  
Resting Membrane Potential ◽  
Lithium Ions

scholarly journals Graded Activation in Frog Muscle Fibers

1973 ◽  
Vol 61 (4) ◽  
pp. 424-443 ◽  
Author(s):  
L. L. Costantin ◽  
S. R. Taylor
Keyword(s):  
Membrane Potential ◽  
Voltage Clamp ◽  
Cross Section ◽  
Muscle Fibers ◽  
Frog Muscle ◽  
Single Muscle ◽  
Fiber Cross Section ◽  
Striation Spacing ◽  
Velocity Of Shortening ◽  
Electrode Voltage

The membrane potential of frog single muscle fibers in solutions containing tetrodotoxin was controlled with a two-electrode voltage clamp. Local contractions elicited by 100-ms square steps of depolarization were observed microscopically and recorded on cinefilm. The absence of myofibrillar folding with shortening to striation spacings below 1.95 µm served as a criterion for activation of the entire fiber cross section. With depolarizing steps of increasing magnitude, shortening occurred first in the most superficial myofibrils and spread inward to involve axial myofibrils as the depolarization was increased. In contractions in which the entire fiber cross section shortened actively, both the extent of shortening and the velocity of shortening at a given striation spacing could be graded by varying the magnitude of the depolarization step. The results provide evidence that the degree of activation of individual myofibrils can be graded with membrane depolarization.

scholarly journals The Suppression of the Late After-Potential in Rubidium-Containing Frog Muscle Fibers

1965 ◽  
Vol 48 (6) ◽  
pp. 1003-1010 ◽  
Author(s):  
D. C. Hellam ◽  
D. A. Goldstein ◽  
L. D. Peachey ◽  
W. H. Freygang
Keyword(s):  
Membrane Potential ◽  
Potassium Concentration ◽  
Muscle Fibers ◽  
Frog Muscle ◽  
Muscle Membrane ◽  
Potassium Permeability ◽  
Intracellular Potassium ◽  
Intracellular Potassium Concentration

The late after-potential that follows trains of impulses in frog muscle fibers is virtually absent when most of the intracellular potassium is replaced by rubidium and the muscle is immersed in rubidium-containing Ringer's fluid. Its amplitude is also reduced in freshly dissected, potassium-containing muscle fibers that are immersed directly in Rb-Ringer's fluid. These findings are discussed in terms of the model for muscle membrane of Adrian and Freygang (1962 a, b) and in relation to the report of Adrian (1964) that Rb-containing muscle fibers do not exhibit the variations in potassium permeability as a function of membrane potential that are found in fibers with normal intracellular potassium concentration immersed in Ringer's fluid.

scholarly journals The Influence of Sodium-Free Solutions on the Membrane Potential of Frog Muscle Fibers

1963 ◽  
Vol 47 (1) ◽  
pp. 117-132 ◽  
Author(s):  
L. J. Mullins ◽  
K. Noda
Keyword(s):  
Membrane Potential ◽  
Activity Coefficients ◽  
Muscle Fibers ◽  
Frog Muscle ◽  
Sartorius Muscle ◽  
Coupling Ratio ◽  
Nernst Equation ◽  
Ringer’S Solution ◽  
Na Efflux ◽  
Frog Sartorius

The membrane potential of frog sartorius muscle fibers in a Cl- and Na-free Ringer's solution when sucrose replaces NaCl is about the same as that in normal Ringer's solution. The K+ efflux is also about the same in the two solutions but muscles lose K and PO4 in sucrose Ringer's solutions. The membrane potential in sucrose Ringer's solution is equal to that given by the Nernst equation for a K+ electrode, when corrections are made for the activity coefficients for K+ inside and outside the fiber. For a muscle in normal Ringer's solution, the measured membrane potential is within a few millivolts of EK. This finding is incompatible with a 1:1 coupled Na-K pump. It is consistent with either no coupling of Na efflux to K influx, or a coupling ratio of 3 or greater.

Effect of hyperosmolarity and furosemide on resting membrane potential and volume of rat skeletal muscle fibers

1989 ◽  
Vol 108 (5) ◽  
pp. 1575-1577 ◽  
Author(s):  
R. F. Sitdikov ◽  
A. Kh Urazaev ◽  
E. M. Volkov ◽  
G. I. Poletaev ◽  
Kh. S. Khamitov
Keyword(s):  
Skeletal Muscle ◽  
Membrane Potential ◽  
Muscle Fibers ◽  
Resting Membrane Potential ◽  
Rat Skeletal Muscle ◽  
Skeletal Muscle Fibers

scholarly journals Voltage modulates halothane-triggered Ca2+ release in malignant hyperthermia-susceptible muscle

2017 ◽  
Vol 150 (1) ◽  
pp. 111-125 ◽  
Author(s):  
Alberto Zullo ◽  
Martin Textor ◽  
Philipp Elischer ◽  
Stefan Mall ◽  
Andreas Alt ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Malignant Hyperthermia ◽  
Time Course ◽  
Voltage Dependence ◽  
Muscle Fibers ◽  
Volatile Anesthetic ◽  
Resting Membrane Potential ◽  
Drug Induced ◽  
Anesthetic Drugs ◽  
Malignant Hyperthermia Susceptible

Malignant hyperthermia (MH) is a fatal hypermetabolic state that may occur during general anesthesia in susceptible individuals. It is often caused by mutations in the ryanodine receptor RyR1 that favor drug-induced release of Ca2+ from the sarcoplasmic reticulum. Here, knowing that membrane depolarization triggers Ca2+ release in normal muscle function, we study the cross-influence of membrane potential and anesthetic drugs on Ca2+ release. We used short single muscle fibers of knock-in mice heterozygous for the RyR1 mutation Y524S combined with microfluorimetry to measure intracellular Ca2+ signals. Halothane, a volatile anesthetic used in contracture testing for MH susceptibility, was equilibrated with the solution superfusing the cells by means of a vaporizer system. In the range 0.2 to 3%, the drug causes significantly larger elevations of free myoplasmic [Ca2+] in mutant (YS) compared with wild-type (WT) fibers. Action potential–induced Ca2+ signals exhibit a slowing of their time course of relaxation that can be attributed to a component of delayed Ca2+ release turnoff. In further experiments, we applied halothane to single fibers that were voltage-clamped using two intracellular microelectrodes and studied the effect of small (10-mV) deviations from the holding potential (−80 mV). Untreated WT fibers show essentially no changes in [Ca2+], whereas the Ca2+ level of YS fibers increases and decreases on depolarization and hyperpolarization, respectively. The drug causes a significant enhancement of this response. Depolarizing pulses reveal a substantial negative shift in the voltage dependence of activation of Ca2+ release. This behavior likely results from the allosteric coupling between RyR1 and its transverse tubular voltage sensor. We conclude that the binding of halothane to RyR1 alters the voltage dependence of Ca2+ release in MH-susceptible muscle fibers such that the resting membrane potential becomes a decisive factor for the efficiency of the drug to trigger Ca2+ release.

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