scholarly journals Excitation-contraction coupling and charge movement in denervated rat extensor digitorum longus and soleus muscles.

1985 ◽  
Vol 358 (1) ◽  
pp. 75-89 ◽  
Author(s):  
A F Dulhunty ◽  
P W Gage
Keyword(s):  
Extensor Digitorum Longus ◽  
Extensor Digitorum ◽  
Charge Movement ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling

Potentiation of the halothane-cooling contractures of mammalian muscles by denervation

1990 ◽  
Vol 68 (9) ◽  
pp. 1207-1213 ◽  
Author(s):  
Margarete M. Trachez ◽  
R. Takashi Sudo ◽  
G. Suarez-Kurtz
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Soleus Muscle ◽  
Extensor Digitorum Longus ◽  
Extensor Digitorum ◽  
Tension Development ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Denervated Muscles

Denervation potentiated the cooling-induced contractures and the halothane-cooling contractures of isolated extensor digitorum longus and soleus muscles of the mouse. These effects were more striking in extensor digitorum longus than in soleus muscles. Significant increases in the peak amplitudes of the halothane-cooling contractures of both muscles and of the cooling contractures of soleus muscle were observed within 2 and 7 days of denervation. The potentiation of the contractures persisted for 90 days, the period of this study. Denervation (>2 days) endowed extensor digitorum longus with the ability to generate cooling contractures in the absence of halothane. The rate of tension development of cooling-induced contractures in the absence or presence of halothane was significantly greater in denervated (2–90 days) than in innervated muscles. Denervation also reduced the effectiveness of procaine in inhibiting the halothane-cooling contractures. It is proposed that the potentiation of cooling-induced contractures in denervated muscles results primarily from an increase in the rate of efflux and in the quantity of Ca2+ released from the sarcoplasmic reticulum, upon cooling and (or) when challenged with halothane.Key words: denervation, excitation–contraction coupling, halothane, cooling-induced contractures, skeletal muscle.

scholarly journals Inactivation of excitation-contraction coupling in rat extensor digitorum longus and soleus muscles.

1988 ◽  
Vol 91 (5) ◽  
pp. 737-757 ◽  
Author(s):  
M Chua ◽  
A F Dulhunty
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Voltage Clamp ◽  
Extensor Digitorum Longus ◽  
Threshold Concentration ◽  
Extensor Digitorum ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Steady State Inactivation ◽  
Spontaneous Relaxation

K contractures and two-microelectrode voltage-clamp techniques were used to measure inactivation of excitation-contraction coupling in small bundles of fibers from rat extensor digitorum longus (e.d.l.) and soleus muscles at 21 degrees C. The rate of spontaneous relaxation was faster in e.d.l. fibers: the time for 120 mM K contractures to decay to 50% of maximum tension was 9.8 +/- 0.5 s (mean +/- SEM) in e.d.l. and 16.8 +/- 1.7 s in soleus. The rate of decay depended on membrane potential: in e.d.l., the 50% decay time was 14.3 +/- 0.7 s for contractures in 80 mM K (Vm = 25 mV) and 4.9 +/- 0.4 s in 160 mM K (Vm = -3 mV). In contrast to activation, which occurred with less depolarization in soleus fibers, steady state inactivation required more depolarization: after 3 min at -40 mV in 40 mM K, the 200 mM K contracture amplitude in e.d.l. fell to 28 +/- 10% (n = 5) of control, but remained at 85 +/- 2% (n = 6) of control in soleus. These different inactivation properties in e.d.l. and soleus fibers were not influenced by the fact that the 200 mM K solution used to test for steady state inactivation produced contractures that were maximal in soleus fibers but submaximal in e.d.l.: a relatively similar depression was recorded in maximal (200 mM K) and submaximal (60 and 80 mM K) contracture tension. A steady state "pedestal" of tension was observed with maintained depolarization after K contracture relaxation and was larger in soleus than in e.d.l. fibers. The pedestal tension was attributed to the overlap between the activation and inactivation curves for tension vs. membrane potential, which was greater in soleus than in e.d.l. fibers. The K contracture results were confirmed with the two-microelectrode voltage clamp: the contraction threshold increased to more positive potentials at holding potentials of -50 mV in e.d.l. or -40 mV in soleus. At holding potentials of -30 mV in e.d.l. or 0 mV in soleus, contraction could not be evoked by 15-ms pulses to +20 mV. Both K contracture and voltage-clamp experiments revealed that activation in soleus fibers occurred with a smaller transient depolarization and was maintained with greater steady state depolarization than in e.d.l. fibers. The K contracture and voltage-clamp results are described by a model in which contraction depends on the formation of a threshold concentration of activator from a voltage-sensitive molecule that can exist in the precursor, activator, or inactive states.

scholarly journals The IQ Motif is Crucial for Cav1.1 Function

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Katarina Stroffekova
Keyword(s):  
Skeletal Muscle ◽  
High Voltage ◽  
Functional Coupling ◽  
Charge Movement ◽  
Excitation Contraction Coupling ◽  
Whole Cell ◽  
Iq Motif ◽  
Contraction Coupling

Ca2+-dependent modulation via calmodulin, with consensus CaM-binding IQ motif playing a key role, has been documented for most high-voltage-activated Ca2+channels. The skeletal muscle Cav1.1 also exhibits Ca2+-/CaM-dependent modulation. Here, whole-cell Ca2+current, Ca2+transient, and maximal, immobilization-resistant charge movement(Qmax)recordings were obtained from cultured mouse myotubes, to test a role of IQ motif in function of Cav1.1. The effect of introducing mutation (IQ to AA) of IQ motif into Cav1.1 was examined. In dysgenic myotubes expressing YFP-Cav1.1AA, neither Ca2+currents nor evoked Ca2+transients were detectable. The loss of Ca2+current and excitation-contraction coupling did not appear to be a consequence of defective trafficking to the sarcolemma. TheQmaxin dysgenic myotubes expressing YFP-Cav1.1AAwas similar to that of normal myotubes. These findings suggest that the IQ motif of the Cav1.1 may be an unrecognized site of structural and functional coupling between DHPR and RyR.

Membranes, calcium, and coupling

1987 ◽  
Vol 65 (4) ◽  
pp. 686-690 ◽  
Author(s):  
R. S. Eisenberg
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Electrical Coupling ◽  
Eukaryotic Cell ◽  
Charge Movement ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Sarcoplasmic Reticulum Membrane ◽  
Voltage Change ◽  
Membrane Compartments ◽  
T System

Every eukaryotic cell contains systems linking the extracellular space and internal membrane compartments. These systems allow cells to communicate and, ultimately they allow the nervous system to control most of the cytoplasmic activity. In skeletal muscle, this system is called "excitation–contraction coupling." While much is known of the early and late steps in coupling, the critical link between the cell (i.e., here the T system) membrane and sarcoplasmic reticulum membrane is not known. Electrical coupling cannot easily account for experimental results; here we show that the Ca2+ influx is not causally related to the excitation–contraction coupling. The most likely mechanism seems to be a variant of the "remote control model" in which a voltage change and accompanying charge movement in the T membrane activates an enzyme tethered to the cytoplasmic leaflet of the T membrane but spanning part of the T – sarcoplasmic reticulum gap.

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