Role of calcium ions and spike activity in the neurotrophic control of membrane potential in rat muscle fibers

1988 ◽  
Vol 19 (4) ◽  
pp. 329-334
Author(s):  
A. Kh. Urazaev ◽  
A. V. Chikin ◽  
E. M. Volkov ◽  
G. I. Poletaev ◽  
Kh. S. Khamitov
Keyword(s):  
Membrane Potential ◽  
Calcium Ions ◽  
Spike Activity ◽  
Muscle Fibers ◽  
Neurotrophic Control ◽  
Rat Muscle

Binding of calcium ions to cell membrane isolated from bullfrog skeletal muscle

1964 ◽  
Vol 207 (2) ◽  
pp. 509-512 ◽  
Author(s):  
K. Koketsu ◽  
R. Kitamura ◽  
R. Tanaka
Keyword(s):  
Skeletal Muscle ◽  
Membrane Potential ◽  
Cell Membrane ◽  
Membrane Permeability ◽  
Calcium Ions ◽  
Cytoplasmic Membrane ◽  
Muscle Fibers ◽  
Potassium Ions ◽  
Chloroform Methanol ◽  
Sodium And Potassium

The membrane fragments of bullfrog skeletal muscle fibers were isolated by a modification of the method of Kono and Colowick (1961). Radiocalcium ions were bound to these isolated membrane fragments, and the binding of calcium ions was impeded by both sodium and potassium ions. The extractable portion of the isolated membrane fragments with chloroform-methanol mixture bound calcium ions whereas no appreciable binding of calcium ions was observed with the extracted residue. The results suggested that the binding of calcium ions takes place on the lipid or lipoprotein of the so-called cytoplasmic membrane which plays an important role in regulating the membrane permeability and the membrane potential.

scholarly journals The Role of Calcium in Excitation-Contraction Coupling of Lobster Muscle

1968 ◽  
Vol 52 (1) ◽  
pp. 88-110 ◽  
Author(s):  
Harold Gainer
Keyword(s):  
Membrane Potential ◽  
Calcium Ions ◽  
Muscle Activation ◽  
Contraction Coupling ◽  
High K ◽  
High Concentrations ◽  
Coupling Mechanisms ◽  
Caffeine Contractures ◽  
Sigmoid Shape

Potassium contractures were induced in lobster muscle bundles under conditions which produced varying KCl fluxes into the fibers. The presence or absence of chloride fluxes during depolarization by high concentrations of potassium, had no effect on the tensions developed. The curve relating tension to the membrane potential had a typical sigmoid shape with an apparent "threshold" for tension at -60 mv. Soaking the muscles in low (0.1 mM) calcium salines for 30 min completely eliminated the potassium contractures but the caffeine contractures were only slightly reduced under these conditions. The potassium contracture could be completely restored in less than 2 min by return of the calcium ions to the saline. Evidence is presented for independent, superficial, and deep calcium sites; the superficial sites appear to be involved in the coupling mechanisms associated with potassium contractures. These sites are highly selective for Ca++, and attempts to substitute either Cd++, Co++, Mg++, Ba++, or Sr++ for Ca++ were unsuccessful. However, K+ appeared to compete with Ca++ for these sites, and the evoked tension could be reduced by prestimulation of the muscle fibers with high K+ salines. The results of studies on the influx of 45Ca during potassium contractures were compatible with the view of muscle activation by the entry of extracellular calcium.

Fusion between myoblasts and adult muscle fibers promotes remodeling of fibers into myotubes in vitro

Development ◽  
1990 ◽  
Vol 109 (1) ◽  
pp. 139-147 ◽  
Author(s):  
T.J. Hinterberger ◽  
K.F. Barald
Keyword(s):  
Satellite Cells ◽  
Adult Mouse ◽  
Muscle Fibers ◽  
Muscle Growth ◽  
Fibroblast Cell ◽  
C2c12 Cells ◽  
Rat Muscle ◽  
Do So

Muscle satellite cells are residual embryonic myoblast precursors responsible for muscle growth and regeneration. In order to examine the role of satellite cells in the initial events of muscle regeneration, we placed individual mature rat muscle fibers in vitro along with their satellite cells. When the satellite cells were allowed to proliferate, they produced populations of myoblasts that fused together to form myotubes on the laminin substrate. These myoblasts and myotubes also fused with the adult fibers. When they did so, the fibers lost their adult morphology, and by 8 days in vitro, essentially all of them were remodeled into structures resembling embryonic myotubes. However, when proliferating satellite cells were eliminated by exposure to cytosine arabinoside (araC), the vast majority of fibers retained their adult shape. Addition of C2C12 cells (a myoblast line derived from adult mouse satellite cells) to araC-treated fiber cultures resulted in their fusion with the rat muscle fibers and restored the ability of the fibers to remodel, whereas addition of either a fibroblast cell line or a transformed, non-fusing variant of C2C12 cells, or addition of conditioned medium from C2C12 cells, failed to do so. These results imply that myoblast fusion is responsible for triggering adult fiber remodeling in vitro.

Blockers of potassium current and resting membrane potential in rat muscle fibers

Life Sciences ◽  
1992 ◽  
Vol 51 (3) ◽  
pp. 235-245 ◽  
Author(s):  
Adriana S. Losavio ◽  
O. Delbono ◽  
S. Muchnik ◽  
B.A. Kotsias
Keyword(s):  
Membrane Potential ◽  
Potassium Current ◽  
Muscle Fibers ◽  
Resting Membrane Potential ◽  
Rat Muscle

Mitochondrial matrix calcium ions regulate energy production in myocardium: A cytochemical study

1990 ◽  
Vol 48 (2) ◽  
pp. 166-167
Author(s):  
W.A. Jacob ◽  
R. Hertsens ◽  
A. Van Bogaert ◽  
M. De Smet
Keyword(s):  
Energy Metabolism ◽  
Calcium Ions ◽  
Energy Production ◽  
Regulation Of Respiration ◽  
Free Calcium ◽  
Mitochondrial Matrix ◽  
Cytochemical Study ◽  
Nmr Techniques

In the past most studies of the control of energy metabolism focus on the role of the phosphorylation potential ATP/ADP.Pi on the regulation of respiration. Studies using NMR techniques have demonstrated that the concentrations of these compounds for oxidation phosphorylation do not change appreciably throughout the cardiac cycle and during increases in cardiac work. Hence regulation of energy production by calcium ions, present in the mitochondrial matrix, has been the object of a number of recent studies.Three exclusively intramitochondnal dehydrogenases are key enzymes for the regulation of oxidative metabolism. They are activated by calcium ions in the low micromolar range. Since, however, earlier estimates of the intramitochondnal calcium, based on equilibrium thermodynamic considerations, were in the millimolar range, a physiological correlation was not evident. The introduction of calcium-sensitive probes fura-2 and indo-1 made monitoring of free calcium during changing energy metabolism possible. These studies were performed on isolated mitochondria and extrapolation to the in vivo situation is more or less speculative.

scholarly journals Intracellular Na+ Modulates Pacemaking Activity in Murine Sinoatrial Node Myocytes: An In Silico Analysis

2021 ◽  
Vol 22 (11) ◽  
pp. 5645
Author(s):  
Stefano Morotti ◽  
Haibo Ni ◽  
Colin H. Peters ◽  
Christian Rickert ◽  
Ameneh Asgari-Targhi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Membrane Potential ◽  
In Silico ◽  
Sinoatrial Node ◽  
In Silico Analysis ◽  
Ankyrin B ◽  
Deficient Mice ◽  
Silico Analysis ◽  
Bursting Activity

Background: The mechanisms underlying dysfunction in the sinoatrial node (SAN), the heart’s primary pacemaker, are incompletely understood. Electrical and Ca2+-handling remodeling have been implicated in SAN dysfunction associated with heart failure, aging, and diabetes. Cardiomyocyte [Na+]i is also elevated in these diseases, where it contributes to arrhythmogenesis. Here, we sought to investigate the largely unexplored role of Na+ homeostasis in SAN pacemaking and test whether [Na+]i dysregulation may contribute to SAN dysfunction. Methods: We developed a dataset-specific computational model of the murine SAN myocyte and simulated alterations in the major processes of Na+ entry (Na+/Ca2+ exchanger, NCX) and removal (Na+/K+ ATPase, NKA). Results: We found that changes in intracellular Na+ homeostatic processes dynamically regulate SAN electrophysiology. Mild reductions in NKA and NCX function increase myocyte firing rate, whereas a stronger reduction causes bursting activity and loss of automaticity. These pathologic phenotypes mimic those observed experimentally in NCX- and ankyrin-B-deficient mice due to altered feedback between the Ca2+ and membrane potential clocks underlying SAN firing. Conclusions: Our study generates new testable predictions and insight linking Na+ homeostasis to Ca2+ handling and membrane potential dynamics in SAN myocytes that may advance our understanding of SAN (dys)function.

Effect of low chloride on relaxation in hamster diaphragm muscle

1986 ◽  
Vol 61 (1) ◽  
pp. 180-184 ◽  
Author(s):  
S. A. Esau ◽  
N. Sperelakis
Keyword(s):  
Membrane Potential ◽  
Muscle Fatigue ◽  
Time Constant ◽  
Diaphragm Muscle ◽  
Resting Membrane Potential ◽  
Krebs Solution ◽  
Sarcolemmal Membrane ◽  
Cl Conductance

With muscle fatigue the chloride (Cl-) conductance of the sarcolemmal membrane decreases. The role of lowered Cl- conductance in the prolongation of relaxation seen with fatigue was studied in isolated hamster diaphragm strips. The muscles were studied in either a Krebs solution or a low Cl- solution in which half of the NaCl was replaced by Na-gluconate. Short tetanic contractions were produced by a 160-ms train of 0.2-ms pulses at 60 Hz from which tension (T) and the time constant of relaxation were measured. Resting membrane potential (Em) was measured using KCl-filled microelectrodes with resistances of 15–20 M omega. Mild fatigue (20% fall in tension) was induced by 24–25 tetanic contractions at the rate of 2/s. There was no difference in Em or T in the two solutions, either initially or with fatigue. The time constant of relaxation was greater in low Cl- solution, both initially (22 +/- 3 vs. 18 +/- 5 ms, mean +/- SD, P less than 0.05) and with fatigue (51 +/- 18 vs. 26 +/- 7 ms, P less than 0.005). Lowering of sarcolemmal membrane Cl- conductance appears to play a role in the slowing of relaxation of hamster diaphragm muscle seen with fatigue.

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