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The plasmalemmal area of striated muscle fibres is greater than the apparent surface area (A = circumference x length) because of variable folds and the invaginations of the caveolae and T-tubules. Freeze-fracture replicas of the surface membrane of sartorius and semitendinosus muscles from Rana pipiens have been used to determine the numbers and(More)
The chemical phosphatase butanedione monoxime (BDM) reversibly inhibited twitches and tetanic contractions in bundles of rat soleus fibres in a dose-dependent manner (2-20 mM) but had no effect on the amplitude or time course of action potentials. In addition, BDM reversibly reduced the amplitude of potassium contractures demonstrating a depressant effect(More)
Asymmetrical charge movements (Q) were recorded from the voltage-clamped ends of muscle fibres in extensor digitorum longus (e.d.l.) and soleus muscles from rats. Tetracaine (2 mM) was added to solutions to prevent contraction. In both muscles the relationship between Q and membrane potential (V) was S-shaped and could be described by the Boltzmann-type(More)
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(More)
1. The steady-state intracellular membrane potential of fibres in thin bundles dissected from mouse extensor digitorum longus or soleus muscles or rat sternomastoid muscles was measured with 3 M-KCl glass micro-electrodes. The steady-state membrane potential was found to depend on the extracellular concentrations of Na, K and Cl ions. 2. The resting(More)
Myotonic dystrophy type 1 (DM1) is a debilitating multisystemic disorder caused by a CTG repeat expansion in the DMPK gene. Aberrant splicing of several genes has been reported to contribute to some symptoms of DM1, but the cause of muscle weakness in DM1 and elevated Ca2+ concentrations in cultured DM muscle cells is unknown. Here, we investigated the(More)
Ca(2+) release from intracellular stores is controlled by complex interactions between multiple proteins. Triadin is a transmembrane glycoprotein of the junctional sarcoplasmic reticulum of striated muscle that interacts with both calsequestrin and the type 1 ryanodine receptor (RyR1) to communicate changes in luminal Ca(2+) to the release machinery.(More)
1. Twitches, tetanic contractions and potassium contractures were recorded isometrically from small bundles of rat soleus muscle fibres. 2. Solutions with reduced calcium concentrations (low-calcium solutions), whether buffered with EGTA (85 and 3 microM-Ca2+) or not (15 microM-Ca2+), caused an initial potentiation of contraction followed by depression. 3.(More)
High-frequency fatigue (HFF), the decline of force during continuous tetanic stimulation (lasting 4-40 s), was studied in isolated bundles of rat skeletal muscle fibers. HFF was slower in slow-twitch soleus fibers than in fast-twitch red or white sternomastoid fibers; denervation accelerated fatigue in soleus. Maximal 200-mmol/L potassium contractures of(More)
Junctin, a non-catalytic splice variant encoded by the aspartate-β-hydroxylase (Asph) gene, is inserted into the membrane of the sarcoplasmic reticulum (SR) Ca(2+) store where it modifies Ca(2+) signalling in the heart and skeletal muscle through its regulation of ryanodine receptor (RyR) Ca(2+) release channels. Junctin is required for normal muscle(More)