scholarly journals EFFECT OF THE LOCAL ANESTHETIC QUATACAINE ON THE MEMBRANE POTENTIAL AND SODIUM CONDUCTANCE OF FROG MUSCLE FIBERS

1972 ◽  
Vol 22 (3) ◽  
pp. 281-293 ◽  
Author(s):  
Norio AKAIKE ◽  
Koitsu NODA
Keyword(s):  
Membrane Potential ◽  
Local Anesthetic ◽  
Muscle Fibers ◽  
Frog Muscle ◽  
Sodium Conductance

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.

Muscle fiber capacity in low conductivity solution

1976 ◽  
Vol 54 (2) ◽  
pp. 107-112 ◽  
Author(s):  
D. Loo ◽  
P. C. Vaughan
Keyword(s):  
Membrane Potential ◽  
Muscle Fiber ◽  
Muscle Fibers ◽  
Circuit Theory ◽  
Frog Muscle ◽  
Constant Current ◽  
Effective Capacity ◽  
Injection Technique ◽  
Length Constant ◽  
Per Se

A method is described for computing the effective capacity of muscle fibers, C = Q/V where Q is the charge stored, and V is the membrane potential, using a standard two-microelectrode, constant current injection technique. The method is used to compare physical (or effective) capacity of frog muscle fibers bathed in a low conductivity, 2.5 mM K+ solution, with circuit-theory derived quantities in the same cells and in control fibers. No differences can be discerned and it is concluded that low conductivity of physiological solutions, per se, does not significantly reduce the length constant of frog muscle transverse tubules.

scholarly journals Globular and asymmetric acetylcholinesterase in frog muscle basal lamina sheaths.

1986 ◽  
Vol 102 (3) ◽  
pp. 762-768 ◽  
Author(s):  
M Nicolet ◽  
M Pinçon-Raymond ◽  
F Rieger
Keyword(s):  
Basal Lamina ◽  
Acetylcholine Receptors ◽  
Muscle Fibers ◽  
Frog Muscle ◽  
Motor Endplate ◽  
Molecular Forms ◽  
Nonionic Detergent ◽  
Plasmic Membrane ◽  
Triton X

After denervation in vivo, the frog cutaneus pectoris muscle can be led to degenerate by sectioning the muscle fibers on both sides of the region rich in motor endplate, leaving, 2 wk later, a muscle bridge containing the basal lamina (BL) sheaths of the muscle fibers (28). This preparation still contains various tissue remnants and some acetylcholine receptor-containing membranes. A further mild extraction by Triton X-100, a nonionic detergent, gives a pure BL sheath preparation, devoid of acetylcholine receptors. At the electron microscope level, this latter preparation is essentially composed of the muscle BL with no attached plasmic membrane and cellular component originating from Schwann cells or macrophages. Acetylcholinesterase is still present in high amounts in this BL sheath preparation. In both preparations, five major molecular forms (18, 14, 11, 6, and 3.5 S) can be identified that have either an asymmetric or a globular character. Their relative amount is found to be very similar in the BL and in the motor endplate-rich region of control muscle. Thus, observations show that all acetylcholinesterase forms can be accumulated in frog muscle BL.

scholarly journals Role of sodium in ADP- and thrombin-induced megakaryocyte spreading.

1983 ◽  
Vol 96 (5) ◽  
pp. 1234-1240 ◽  
Author(s):  
R M Leven ◽  
W H Mullikin ◽  
V T Nachmias
Keyword(s):  
Membrane Potential ◽  
Intracellular Recording ◽  
Membrane Depolarization ◽  
Sodium Permeability ◽  
Sodium Conductance ◽  
Extracellular Sodium

We investigated the role of sodium in megakaryocyte spreading induced by thrombin and ADP. We found that if extracellular sodium was replaced by lithium, potassium, or choline, spreading was inhibited. When extracellular sodium was present, amiloride or tetrodotoxin inhibited spreading. Using intracellular recording we found spreading to be associated with a permanent membrane depolarization. The extent and rate of thrombin-induced depolarization was reduced when lithium replaced sodium. Unspread cells had an average membrane potential of -44.8 mV. Spread cells had an average membrane potential of -18.46 mV. When choline replaced sodium, or when in the presence of tetrodotoxin and amiloride, the spread cells repolarized, indicating that the depolarization is due to an increase in sodium permeability. Similar treatments did not change the membrane potential of unspread cells. Incubation of megakaryocytes with A23187 together with monensin or methylamine induced spreading. Methylamine occasionally caused spreading by itself, but neither ionophore alone caused spreading. These results indicate that megakaryocyte spreading induced by ADP and thrombin depends on an increase in sodium conductance.

Inhibition of Zn2+-induced potentiation of twitch tension by Ni2+ in frog muscle

1986 ◽  
Vol 64 (5) ◽  
pp. 625-630
Author(s):  
Toshiharu Oba ◽  
Ken Hotta
Keyword(s):  
Action Potential ◽  
Inhibitory Action ◽  
Channel Blocker ◽  
Rana Catesbeiana ◽  
Muscle Fibers ◽  
Frog Muscle ◽  
Duration Of Action ◽  
Ringer’S Solution ◽  
Mechanical Threshold ◽  
T Tubules

Effect of Ni2+ on Zn2+-induced potentiation of twitch tension was studied electrophysiologically in the toe muscle fibers of Rana catesbeiana. The major findings of this investigation are as follows. When 2 mM Ni2+ was applied to fibers in a normal Ringer's solution containing 50 μM Zn2+ (Zn2+ solution), the Zn2+-potentiated twitch tension decreased remarkably to about one-third of that before Ni2+ treatment. This concentration of Ni2+ caused a 23% decrease in the duration of action potential which had been prolonged by Zn2+ (6.61–5.09 ms). Ni2+ (2 mM) added to normal Ringer's solution led to increases of about 30 and 42% in twitch tension and in the duration of action potential, respectively. A slight increase in the mechanical threshold was induced by 2 mM Ni2+. The inhibitory action of Ni2+ on the twitch tension in Zn2+ solution was larger than that in the case of tetanus tension. Diltiazem (40 μM), aCa2+ channel blocker, did not inhibit the twitch tension potentiated in Zn2+ solution. These results suggest that the decrease in Zn2+-potentiated twitch tension by Ni2+ may possibly derive from impairment of the propagation of action potential along the T tubules.

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