scholarly journals Length-dependent electromechanical coupling in single muscle fibers.

1976 ◽  
Vol 68 (6) ◽  
pp. 653-669 ◽  
Author(s):  
A M Gordon ◽  
E B Ridgway

In single muscle fibers from the giant barnacle, a small decrease in muscle length decreases both the calcium activation and the peak isometric tension produced by a constant current stimulus. The effect is most pronounced if the length change immediately precedes the stimulation. In some cases, the decrease in tension with shortening can be accounted for almost entirely by a decrease in calcium release rather than changes in mechanical factors such as filament geometry. During the constant current stimulation the muscle membrane becomes more depolarized at longer muscle lengths than at the shorter muscle lengths. Under voltage clamp conditions, when the membrane potential is kept constant during stimulation, there is little length dependence of calcium release. Thus, the effect of length on calcium release is mediated through a change in membrane properties, rather than an effect on a subsequent step in excitation-contraction coupling. Stretch causes the unstimulated fiber membrane to depolarize by about l mV while release causes the fiber membrane to hyperpolarize by about the same amount. The process causing this change in potential has an equilibrium potential nearly 10 mV hyperpolarized from the resting level. This change in resting membrane potential with length may account for the length dependence of calcium release.

1964 ◽  
Vol 48 (2) ◽  
pp. 225-234 ◽  
Author(s):  
Charles Edwards ◽  
Shiko Chichibu ◽  
Susumu Hagiwara

Constant current pulses have been applied to single muscle fibers of the barnacle, Balanus nubilus Darwin, with an axial metal electrode. The membrane potential change, which took place over a large part of the muscle fiber, was measured with a similar electrode. Depolarizing pulses, if the voltage was greater than threshold, produced tension. The size of the tension was a function of the magnitude and the duration of the depolarizing pulses. The latency between the onset of depolarization and tension can be only in part attributable to mechanical factors. AC stimulation produced tension, but 5 to 10 seconds were required for the steady-state level of the tension to be reached. Muscles were depolarized in elevated K and studied after the contracture had terminated. If not too depolarized, further depolarization produced tension. Termination of hyperpolarizing pulses also produced tension, which decayed quite slowly. Hyperpolarizing pulses reduced, or abolished, any preexisting tension. Thus, it appears that at certain values of the membrane potential tension is set up, but there is also a slow process of accommodation present.


1973 ◽  
Vol 61 (4) ◽  
pp. 424-443 ◽  
Author(s):  
L. L. Costantin ◽  
S. R. Taylor

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.


1965 ◽  
Vol 48 (6) ◽  
pp. 1003-1010 ◽  
Author(s):  
D. C. Hellam ◽  
D. A. Goldstein ◽  
L. D. Peachey ◽  
W. H. Freygang

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.


1994 ◽  
Vol 71 (2) ◽  
pp. 656-665 ◽  
Author(s):  
T. Yagi ◽  
P. R. Macleish

1. The membrane properties of cone inner segments dissociated enzymatically from monkey retina were studied under voltage-clamp conditions using patch pipettes in the whole-cell clamp configuration. 2. A noninactivating, voltage-gated calcium current was evoked at potentials positive to -60 mV and peaked between -30 and -20 mV when barium was substituted for calcium. Cadmium (50 microM) but not nickel (50 microM) blocked the current. 3. A large calcium-activated anion current (IAn) was observed when the membrane potential was set to a level between -60 and 30 mV. The reversal potential of IAn was 0 mV with chloride as the sole anion and about -30 and -40 mV when methanesulfonate and D-aspartate, respectively, replaced intracellular chloride to set the equilibrium potential for chloride at -50 mV. IAn inactivated and oscillated when the membrane potential was maintained at depolarized levels, contrary to calcium-activated anionic currents seen in photoreceptors of other species. 4. A sustained-type potassium current was activated by depolarizations positive to -50 mV. The time course of activation and deactivation were voltage dependent. This potassium current was partially blocked by 20 mM tetraethylammonium ions. 5. A transient potassium current was activated by depolarizations positive to -20 mV. This current was blocked by 4-aminopyridine (2 mM) and inactivated with a time constant of approximately 500 ms. The amplitude in response to voltage steps to 45 mV was decreased by prepulses to voltages more positive than -30 mV. 6. Hyperpolarization negative to -65 mV activated an inward current that was completely blocked by external cesium (10 mM). The reversal potential suggested a conductance mechanism permeable to both sodium and potassium ions. 7. A calcium-activated potassium current, which was found in salamander photoreceptors, was not detected. 8. The presence of these conductances is expected to influence the membrane potential and the time course of the light response in monkey cones.


2016 ◽  
Vol 147 (4) ◽  
pp. 291-308 ◽  
Author(s):  
Thomas Holm Pedersen ◽  
Anders Riisager ◽  
Frank Vincenzo de Paoli ◽  
Tsung-Yu Chen ◽  
Ole Bækgaard Nielsen

Electrical membrane properties of skeletal muscle fibers have been thoroughly studied over the last five to six decades. This has shown that muscle fibers from a wide range of species, including fish, amphibians, reptiles, birds, and mammals, are all characterized by high resting membrane permeability for Cl− ions. Thus, in resting human muscle, ClC-1 Cl− ion channels account for ∼80% of the membrane conductance, and because active Cl− transport is limited in muscle fibers, the equilibrium potential for Cl− lies close to the resting membrane potential. These conditions—high membrane conductance and passive distribution—enable ClC-1 to conduct membrane current that inhibits muscle excitability. This depressing effect of ClC-1 current on muscle excitability has mostly been associated with skeletal muscle hyperexcitability in myotonia congenita, which arises from loss-of-function mutations in the CLCN1 gene. However, given that ClC-1 must be drastically inhibited (∼80%) before myotonia develops, more recent studies have explored whether acute and more subtle ClC-1 regulation contributes to controlling the excitability of working muscle. Methods were developed to measure ClC-1 function with subsecond temporal resolution in action potential firing muscle fibers. These and other techniques have revealed that ClC-1 function is controlled by multiple cellular signals during muscle activity. Thus, onset of muscle activity triggers ClC-1 inhibition via protein kinase C, intracellular acidosis, and lactate ions. This inhibition is important for preserving excitability of working muscle in the face of activity-induced elevation of extracellular K+ and accumulating inactivation of voltage-gated sodium channels. Furthermore, during prolonged activity, a marked ClC-1 activation can develop that compromises muscle excitability. Data from ClC-1 expression systems suggest that this ClC-1 activation may arise from loss of regulation by adenosine nucleotides and/or oxidation. The present review summarizes the current knowledge of the physiological factors that control ClC-1 function in active muscle.


1968 ◽  
Vol 46 (1) ◽  
pp. 1-9 ◽  
Author(s):  
H. L. Atwood

The effects of bromide, nitrate, iodide, and thiocyanate ions on the neurally evoked fast and slow contractions of a crab muscle were investigated. Both types of contraction were depressed in bromide and nitrate. In iodide and thiocyanate, the slow contraction was often depressed but the fast contraction was potentiated. The foreign anions increased muscle fiber membrane resistance and the amplitudes of both fast and slow postsynaptic potentials. Records of tension development in single muscle fibers showed that more stimulating current was required to produce a given tension in nitrate than in the standard bathing fluid; this change was related to hyperpolarization of the muscle fiber membrane in nitrate. Potassium contractures also were inhibited by nitrate, because of the less effective depolarization of the cell membrane by potassium ion in the presence of nitrate. No marked shift in the membrane potential threshold for contraction occurred after treatment with the foreign anions.


1982 ◽  
Vol 243 (6) ◽  
pp. E512-E521 ◽  
Author(s):  
R. L. Ruff ◽  
D. Martyn ◽  
A. M. Gordon

We explored the possibility that glucocorticoid-induced muscle weakness and atrophy resulted from impaired muscle membrane excitability. Male Sprague-Dawley rats received intramuscular injections of dexamethasone, cortisone acetate (equivalent anti-inflammatory doses), or saline for up to 28 days. Temporal patterns of change in muscle mass, twitch and tetanic tension, and membrane potential, cable parameters, and excitability were studied in vitro in the extensor digitorum longus (EDL), soleus (SOL), omohyoid (OMO), caudofemoralis (CF), and the sternomastoid muscles (membrane potential only). the membrane properties of EDL fibers were also studied in vivo (pentobarbital anesthesia). The relative severity of atrophy was OMO greater than CF greater than EDL greater than SOL. Reduction in twitch or tetanic tension never preceded atrophy. The twitch and tetanic tension (per g muscle) increased with glucocorticoid treatment. There were no significant changes in the time course of the twitch or tetanus. Dexamethasone produced more severe atrophy and force reduction than did cortisone acetate. Glucocorticoid treatment produced a depolarization of EDL muscle fibers measured in vitro at 23 degrees C, but this did not appear to be physiologically significant because EDL fibers studied in vivo were not depolarized and had normal action potential amplitudes and thresholds. Glucocorticoid treatment did not change the membrane resistance or capacitance. We conclude that glucocorticoid treatment did not produce muscle weakness by impairing sarcolemmal excitability or excitation-contraction coupling, but that the weakness resulted from muscle atrophy.


1959 ◽  
Vol 43 (2) ◽  
pp. 377-395 ◽  
Author(s):  
J. A. Cerf ◽  
H. Grundfest ◽  
G. Hoyle ◽  
Frances V. McCann

Dually innervated Romalea muscle fibers which respond differently to stimulation of their fast and slow axons are excited by intracellularly applied depolarizing stimuli. The responses, though spike-like in appearance, are graded in amplitude depending upon the strength of the stimuli and do not exceed about 30 mv. in height. In other respects, however, these graded responses possess properties that are characteristic of electrically excitable activity: vanishingly brief latency; refractoriness; a post-spike undershoot. They are blocked by hyperpolarizing the fiber membrane; respond repetitively to prolonged depolarization, and are subject to depolarizing inactivation. As graded activity, these responses propagate decrementally. The fast and slow axons of the dually responsive muscle fibers initiate respectively large and small postsynaptic potentials (p.s.p.'s) in the muscle fiber. These responses possess properties that characterize electrically inexcitable depolarizing activity. They are augmented by hyperpolarization and diminished by depolarization. Their latency is independent of the membrane potential. They have no refractory period, thus being capable of summation. The fast p.s.p. evokes a considerable or maximal electrically excitable response. The combination, which resembles a spike, leads to a twitch-like contraction of the muscle fiber. The individual slow p.s.p.'s elicit no or only little electrically excitable responses, and they evoke slower smaller contractile responses. The functional aspects of dual responsiveness and the several aspects of the theoretical importance of the gradedly responsive, electrically excitable component are discussed.


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