Excitation–contraction coupling in crab muscle fibers with swollen T tubules

1985 ◽  
Vol 63 (7) ◽  
pp. 879-885 ◽  
Author(s):  
J. H. Leal-Cardoso ◽  
G. Suarez-Kurtz
Keyword(s):  
Time Course ◽  
Membrane Conductance ◽  
Membrane Resistance ◽  
Membrane Properties ◽  
Membrane Excitability ◽  
High Potassium ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Voltage Dependent ◽  
T Tubules

Single crab (Callinectes danae) fibers were equilibrated with isotonic, high KC1 solutions and were subsequently returned to the control saline. This caused marked swelling of the T tubules. Fibers treated with 100 mM KCl had a 2.5-mV residual depolarization, a 50% decrease in effective membrane resistance (Reff) and a 75% reduction in membrane time constant (τm). These fibers exhibited large increases in membrane conductance upon depolarization and were inexcitable; membrane depolarization with current pulses elicited no contraction. The effects of the KCl treatment on membrane properties were not reproduced by treatment with high potassium gluconate solutions, which did not cause tubular swelling. Tetrabutylammonium (10 mM) or Ba ions (10–20 mM), but not tetraethylammonium (40–100 mM), Sr ions (15–70 mM), or procaine (1–8 mM) reversed the effects of the KCl treatment on Reff, τm, membrane excitability, and excitation–contraction coupling. The time course of the Ba effects was consistent with the suggestion that the KCl treatment increases the K conductance of the tubular membranes, which in turn prevents the activation of voltage-dependent Ca channels located in the membranes of the T system. This results in inhibition of the Ca-dependent electrogenesis and consequently, the absence of contraction upon depolarization of the plasma membrane.

Temperature Effects on Neuromuscular Transmission (Opener Muscle of Crayfish, Astacus Leptodactylus)

1981 ◽  
Vol 94 (1) ◽  
pp. 251-268
Author(s):  
LUDWIG FISCHER ◽  
ERNST FLOREY
Keyword(s):  
Decay Time ◽  
Neuromuscular Transmission ◽  
Membrane Conductance ◽  
Resting Potential ◽  
Muscle Fibres ◽  
Astacus Leptodactylus ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Temperature Range ◽  
Parallel Change

In experiments on the opener muscle of the third walking legs of crayfish (Astacus leptodactylus) it was found that the mechanical tension developed in response to repetitive stimulation of the single motor axon increases over the entire temperature range from 30 down to 0°C. In contrast to this, the tension elicited by depolarizing single muscle fibres decreases with decreasing temperature; the threshold for excitation-contraction coupling is not significantly altered. With decreasing temperature the resting potential decreases (up to 2 mV/°C) but the amplitude and decay time of the e.p.s.p.'s increase. The time constant, λ, of e.p.s.p. decay has a Q10 of less than −2 in the range above 15 °C but reaches a value of −7 between 10 and 0°C. This pattern of temperature dependence is fully accounted for by a parallel change of membrane resistance and its reciprocal, the membrane conductance. The corresponding activation energies computed from λ-values approximate 3 kcal/mol at high temperature and 46 kcal/mol in the low temperature range. The combined effects of a lowered resting potential, an increased amplitude, and especially an increased decay time of e.p.s.p.s result in a drastic enhancement of the depolarization reached during summation of e.p.s.p.s as the temperature is decreased. These effects overcompensate the declining effectiveness of excitation-contraction coupling so that the entire process of neuromuscular transmission becomes more and more effective as the temperature declines. In order to reach the same tension lower frequencies of nerve stimulation are needed at lower temperatures.

Ba2+, TEA+, and quinine effects on apical membrane K+ conductance and maxi K+ channels in gallbladder epithelium

1990 ◽  
Vol 259 (1) ◽  
pp. C56-C68 ◽  
Author(s):  
Y. Segal ◽  
L. Reuss
Keyword(s):  
Apical Membrane ◽  
Membrane Conductance ◽  
Membrane Resistance ◽  
K Channel ◽  
Dependent Manner ◽  
Gallbladder Epithelium ◽  
Concentration Dependent Manner ◽  
K Channels ◽  
Voltage Dependent ◽  
Channel Currents

The apical membrane of Necturus gallbladder epithelium contains a voltage-activated K+ conductance [Ga(V)]. Large-conductance (maxi) K+ channels underlie Ga(V) and account for 17% of the membrane conductance (Ga) under control conditions. We examined the Ba2+, tetraethylammonium (TEA+), and quinine sensitivities of Ga and single maxi K+ channels. Mucosal Ba2+ addition decreased resting Ga in a concentration-dependent manner (65% block at 5 mM) and decreased Ga(V) in a concentration- and voltage-dependent manner. Mucosal TEA+ addition also decreased control Ga (60% reduction at 5 mM). TEA+ block of Ga(V) was more potent and less voltage dependent that Ba2+ block. Maxi K+ channels were blocked by external Ba2+ at millimolar levels and by external TEA+ at submillimolar levels. At 0.3 mM, quinine (mucosal addition) hyperpolarized the cell membranes by 6 mV and reduced the fractional apical membrane resistance by 50%, suggesting activation of an apical membrane K+ conductance. At 1 mM, quinine both activated and blocked K(+)-conductive pathways. Quinine blocked maxi K+ channel currents at submillimolar concentrations. We conclude that 1) Ba2+ and TEA+ block maxi K+ channels and other K+ channels underlying resting Ga; 2) parallels between the Ba2+ and TEA+ sensitivities of Ga(V) and maxi K+ channels support a role for these channels in Ga(V); and 3) quinine has multiple effects on K(+)-conductive pathways in gallbladder epithelium, which are only partially explained by block of apical membrane maxi K+ channels.

Segment-specific effects of FMRFamide on membrane properties of heart interneurons in the leech

1995 ◽  
Vol 74 (4) ◽  
pp. 1485-1497 ◽  
Author(s):  
J. Schmidt ◽  
S. Gramoll ◽  
R. L. Calabrese
Keyword(s):  
Outward Current ◽  
Membrane Conductance ◽  
Membrane Properties ◽  
Inward Current ◽  
Specific Effects ◽  
Outward Currents ◽  
Voltage Dependent ◽  
Inward Currents ◽  
K Current ◽  
Conductance Increase

1. The effects of Phe-Met-Arg-Phe (FMRF)amide (10(-6) M) on membrane properties of heart interneurons in the third, fourth, and fifth segmental ganglia [HN(3), HN(4), and HN(5) cells, respectively] of the leech were studied using discontinuous current-clamp and single-electrode voltage-clamp techniques. FMRFamide was focally applied onto the soma of the cell under investigation. 2. Application of FMRFamide depolarized HN(3) and HN(4) cells by evoking an inward current. These responses were subject to pronounced desensitization. The inward currents evoked by application of FMRFamide were associated with an increase in membrane conductance and appeared to be voltage dependent. Currents were enhanced at more depolarized potentials. 3. The responsiveness of the HN(3) and HN(4) cells was not affected when the Ca2+ concentration in the bath saline was reduced from normal (1.8 mM) to 0.1 mM. The depolarizing response on application of FMRFamide was blocked when Co2+ was substituted for Ca2+. 4. HN(3) and HN(4) cells did not respond to FMRFamide application in Na(+)-free solution. Inward currents were largely reduced when bath saline with 30% of the normal Na+ concentration was used. When Li+ was substituted for Na+ in the saline, application of FMRFamide still evoked depolarizing responses in HN(3) and HN(4) cells. 5. We conclude that focal application of FMRFamide onto the somata of HN(3) and HN(4) cells evokes a voltage-dependent inward current, carried largely by Na+. 6. Focal application of FMRFamide onto somata of HN(5) cells hyperpolarized these cells by activating a voltage-dependent outward current. 7. HN(5) cells were loaded with Cl- until inhibitory postsynaptic potentials carried by Cl- reversed. Cl(-)-loaded cells still responded with a hyperpolarization when FMRFamide was applied onto their somata. Therefore the outward current evoked by FMRFamide appears to be mediated by a K+ conductance increase. 8. Application of FMRFamide onto the somata of HN(5) cells enhanced outward currents that were evoked by depolarizing voltage steps from a holding potential of -45 mV. 9. We conclude that the hyperpolarizing response of HN(5) cells to focal application of FMRFamide onto their somata is the result of an up-regulation of a voltage-dependent K+ current.

Calmodulin and Excitation-Contraction Coupling

Physiology ◽  
2000 ◽  
Vol 15 (6) ◽  
pp. 281-284 ◽  
Author(s):  
Susan L. Hamilton ◽  
Irina Serysheva ◽  
Gale M. Strasburg
Keyword(s):  
Skeletal Muscle ◽  
Ion Channels ◽  
Sarcoplasmic Reticulum ◽  
Release Channel ◽  
Excitation Contraction Coupling ◽  
Transverse Tubule ◽  
Contraction Coupling ◽  
Voltage Dependent ◽  
Important Regulator ◽  
Precise Role

Excitation-contraction coupling in cardiac and skeletal muscle involves the transverse-tubule voltage-dependent Ca2+ channel and the sarcoplasmic reticulum Ca2+ release channel. Both of these ion channels bind and are modulated by calmodulin in both its Ca2+-bound and Ca2+-free forms. Calmodulin is, therefore, potentially an important regulator of excitation-contraction coupling. Its precise role, however, has not yet been defined.

Ionic mechanisms and Ca2+ regulation in airway smooth muscle contraction: do the data contradict dogma?

2002 ◽  
Vol 282 (6) ◽  
pp. L1161-L1178 ◽  
Author(s):  
Luke J. Janssen
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Smooth Muscle Contraction ◽  
Channel Blockers ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Spatial And Temporal Heterogeneity ◽  
Voltage Dependent ◽  
Intracellular Ca ◽  
Ionic Mechanisms

In general, excitation-contraction coupling in muscle is dependent on membrane depolarization and hyperpolarization to regulate the opening of voltage-dependent Ca2+ channels and, thereby, influence intracellular Ca2+ concentration ([Ca2+]i). Thus Ca2+ channel blockers and K+ channel openers are important tools in the arsenals against hypertension, stroke, and myocardial infarction, etc. Airway smooth muscle (ASM) also exhibits robust Ca2+, K+, and Cl− currents, and there are elaborate signaling pathways that regulate them. It is easy, then, to presume that these also play a central role in contraction/relaxation of ASM. However, several lines of evidence speak to the contrary. Also, too many researchers in the ASM field view the sarcoplasmic reticulum as being centrally located and displacing its contents uniformly throughout the cell, and they have focused almost exclusively on the initial single [Ca2+] spike evoked by excitatory agonists. Several recent studies have revealed complex spatial and temporal heterogeneity in [Ca2+]i, the significance of which is only just beginning to be appreciated. In this review, we will compare what is known about ion channels in ASM with what is believed to be their roles in ASM physiology. Also, we will examine some novel ionic mechanisms in the context of Ca2+ handling and excitation-contraction coupling in ASM.

scholarly journals Modelling depolarization delay, sodium currents, and electrical potentials in cardiac transverse tubules

2019 ◽  
Author(s):  
Sarah H. Vermij ◽  
Hugues Abriel ◽  
Jan P. Kucera
Keyword(s):  
Striated Muscle ◽  
Sodium Current ◽  
Cardiac Cells ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Tubular Membrane ◽  
Electrical Potentials ◽  
Tubular Lumen ◽  
T Tubules ◽  
Extracellular Potentials

ABSTRACTT-tubules are invaginations of the lateral membrane of striated muscle cells that provide a large surface for ion channels and signaling proteins, thereby supporting excitation-contraction coupling. T-tubules are often remodeled in heart failure. To better understand the electrical behavior of T-tubules of cardiac cells in health and disease, this study addresses two largely unanswered questions regarding their electrical properties: (1) the delay of T-tubular membrane depolarization and (2) the effects of T-tubular sodium current on T-tubular potentials.Here, we present an elementary computational model to determine the delay in depolarization of deep T-tubular membrane segments as the narrow T-tubular lumen provides resistance against the extracellular current. We compare healthy tubules to tubules with constrictions and diseased tubules from mouse and human, and conclude that constrictions greatly delay T-tubular depolarization, and diseased T-tubules depolarize faster than healthy ones due to tubule widening. We moreover model the effect of T-tubular sodium current on intraluminal T-tubular potentials. We observe that extracellular potentials become negative during the sodium current transient (up to −50 mV in constricted T-tubules), which feedbacks on sodium channel function (self-attenuation) in a manner resembling ephaptic effects that have been described for intercalated discs where opposing membranes are very close together.These results show that (1) the excitation-contraction coupling defects seen in diseased cells cannot be explained by T-tubular remodeling alone; and (2) the sodium current may modulate intraluminal potentials. Such extracellular potentials might also affect excitation-contraction coupling.

Ionic conductances of monkey solitary cone inner segments

1994 ◽  
Vol 71 (2) ◽  
pp. 656-665 ◽  
Author(s):  
T. Yagi ◽  
P. R. Macleish
Keyword(s):  
Membrane Potential ◽  
Potassium Current ◽  
Time Course ◽  
Reversal Potential ◽  
Light Response ◽  
Membrane Properties ◽  
Equilibrium Potential ◽  
Ionic Conductances ◽  
Voltage Dependent ◽  
Tetraethylammonium Ions

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.

Junctional Sarcoplasmic Reticulum in Excitation-Contraction-Coupling

1982 ◽  
Vol 40 ◽  
pp. 136-137
Author(s):  
J.R. Sommer ◽  
E. Bossen ◽  
A. Fabiato
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Action Potential ◽  
Muscle Contraction ◽  
Cardiac Cells ◽  
Close Apposition ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Terminal Cisterna ◽  
Voltage Dependent ◽  
Junctional Sarcoplasmic Reticulum

The junctional sarcoplasmic reticulum (JSR, syn. terminal cisterna) is implicated in Ca++storage and release for muscle contraction. Its discrete ultrastructure permits distinction from the rest of the SR (free SR) even when it occurs without plasmalemmal contact, e.g. as extended JSR (EJSR) in bird, and corbular SR (CSR) in mammalian cardiac cells. The close apposition of JSR to plasmalemma via junctional processes is central to proposed mechanisms of translating voltage-dependent charge transfers at the plasmalemma during the action potential into Ca++release from the JSR. These hypotheses are put into question by the existence of EJSR (and CSR) which in birds constitutes 70-80% of the total JSR. An alternate hypothesis proposes, at least for cardiac cells, that Ca++entering the cell during excitation causes additional Ca++to be freed intracellularly. The notion of a chemical transmitter acting by diffusion is attractive because it will allow for the anomalous topography of EJSR, especially since bird cardiac cells have only about half the diameter of their mammalian relatives and have no transverse tubules.

scholarly journals Ca2+ cycling in cardiomyocytes from a high-performance reptile, the varanid lizard (Varanus exanthematicus)

2009 ◽  
Vol 297 (6) ◽  
pp. R1636-R1644 ◽  
Author(s):  
Gina L. J. Galli ◽  
Daniel E. Warren ◽  
Holly A. Shiels
Keyword(s):  
Sarcoplasmic Reticulum ◽  
High Performance ◽  
Time Course ◽  
Ventricular Myocytes ◽  
Volume Ratio ◽  
Voltage Sensitivity ◽  
Excitation Contraction Coupling ◽  
Electrophysiological Properties ◽  
Contraction Coupling ◽  
Cardiovascular Performance

The varanid lizard possesses one of the largest aerobic capacities among reptiles with maximum rates of oxygen consumption that are twice that of other lizards of comparable sizes at the same temperature. To support this aerobic capacity, the varanid heart possesses morphological adaptations that allow the generation of high heart rates and blood pressures. Specializations in excitation-contraction coupling may also contribute to the varanids superior cardiovascular performance. Therefore, we investigated the electrophysiological properties of the l-type Ca2+ channel and the Na+/Ca2+ exchanger (NCX) and the contribution of the sarcoplasmic reticulum to the intracellular Ca2+ transient (Δ[Ca2+]i) in varanid lizard ventricular myocytes. Additionally, we used confocal microscopy to visualize myocytes and make morphological measurements. Lizard ventricular myocytes were found to be spindle-shaped, lack T-tubules, and were ∼190 μm in length and 5–7 μm in width and depth. Cardiomyocytes had a small cell volume (∼2 pL), leading to a large surface area-to-volume ratio (18.5), typical of ectothermic vertebrates. The voltage sensitivity of the l-type Ca2+ channel current ( ICa), steady-state activation and inactivation curves, and the time taken for recovery from inactivation were also similar to those measured in other reptiles and teleosts. However, transsarcolemmal Ca2+ influx via reverse mode Na+/Ca2+ exchange current was fourfold higher than most other ectotherms. Moreover, pharmacological inhibition of the sarcoplasmic reticulum led to a 40% reduction in the Δ[Ca2+]i amplitude, and slowed the time course of decay. In aggregate, our results suggest varanids have an enhanced capacity to transport Ca2+ through the Na+/Ca2+ exchanger, and sarcoplasmic reticulum suggesting specializations in excitation-contraction coupling may provide a means to support high cardiovascular performance.

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