scholarly journals Influence of phospholipase C on some electrical properties of the skeletal muscle membrane

1967 ◽  
Vol 190 (1) ◽  
pp. 123-137 ◽  
Author(s):  
E. X. Albuquerque ◽  
S. Thesleff
1974 ◽  
Vol 52 (4) ◽  
pp. 887-890 ◽  
Author(s):  
L. L. Odette ◽  
H. L. Atwood

The effect of dantrolene sodium, a muscle relaxant effective on vertebrate skeletal muscle, has been studied on the stretcher muscle of a crab (Callinectes sapidus). The drug rapidly and reversibly attenuates the muscle contractile response to direct and indirect stimulation. Neuromuscular transmission is unaffected, as are the electrical properties of the muscle membrane. It is concluded that dantrolene sodium uncouples excitation–contraction mechanisms in crustacean tonic muscle.


1966 ◽  
Vol 44 (5) ◽  
pp. 791-802 ◽  
Author(s):  
M. H. Sherebrin ◽  
A. C. Burton

The resting potential of single cells in the flexor thigh muscles of rats was measured in an attempt to find a change in the electrical properties of the cell membrane with cold acclimation, in order to identify and relate metabolic changes occurring with non-shivering thermogenesis. The mean resting potential of cells in cold-acclimated rats was found to be slightly but significantly higher than in the controls. A larger temperature gradient with depth was measured in the cold-acclimated animals than in the controls. If the Q10 of resting potential with temperature is as great as 1.16, the higher potential in the cold-acclimated rats may be accounted for by this temperature difference. The resting potential was also found to vary with depth in both groups of rats. This could not be attributed to temperature gradients, and change from red to white muscle cells with depth is thought to be the main factor for the increase of potential with depth.


2010 ◽  
Vol 109 (3) ◽  
pp. 901-905 ◽  
Author(s):  
Bingjing Wang ◽  
Zhaohui Yang ◽  
Becky K. Brisson ◽  
Huisheng Feng ◽  
Zhiqian Zhang ◽  
...  

Mutations that result in the loss of the protein dysferlin result in defective muscle membrane repair and cause either a form of limb girdle muscular dystrophy (type 2B) or Miyoshi myopathy. Most patients are compound heterozygotes, often carrying one allele with a nonsense mutation. Using dysferlin-deficient mouse and human myocytes, we demonstrated that membrane blebbing in skeletal muscle myotubes in response to hypotonic shock requires dysferlin. Based on this, we developed an in vitro assay to assess rescue of dysferlin function in skeletal muscle myotubes. This blebbing assay may be useful for drug discovery/validation for dysferlin deficiency. With this assay, we demonstrate that the nonsense suppression drug, ataluren (PTC124), is able to induce read-through of the premature stop codon in a patient with a R1905X mutation in dysferlin and produce sufficient functional dysferlin (∼15% of normal levels) to rescue myotube membrane blebbing. Thus ataluren is a potential therapeutic for dysferlin-deficient patients harboring nonsense mutations.


1974 ◽  
Vol 52 (6) ◽  
pp. 1126-1135 ◽  
Author(s):  
D. J. Parry ◽  
A. Kover ◽  
G. B. Frank

Exposure of frog toe muscles to 1 mM La3+ results in a decrease in amplitude and rate of tension development of potassium contractures and twitches. At this concentration La3+ also inhibits the uptake of calcium, both in the resting condition and during stimulation. Caffeine contractures are unaffected even after a 5-min pre-exposure to La3+. The depolarization induced by various concentrations of K+ is reduced by about 10 mV as is the amplitude of the action potential. The rate of rise of the action potential is reduced by about 40% after 1 min in La3+ Ringer. Neither the decreased amplitude nor the reduced rate of depolarization is considered to be sufficient to explain the inhibition of tension development. It is suggested that La3+ partially uncouples excitation from contraction by preventing the release of a trigger-Ca2+ fraction from some site on the muscle membrane. This fraction normally plays a role in excitation–contraction coupling, although some tension may still be developed in the absence of a trigger-Ca2+ influx.


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