Changes in isometric contractile properties of fast-twitch and slow-twitch skeletal muscle of dystrophic mice during postnatal development

Bressler, Bernard; Jasch, Laura G.; Ovalle, William K.; Slonecker, Charles E.

doi:10.1016/0014-4886(83)90297-2

Cited by 22 publications

(4 citation statements)

References 25 publications

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“…As mentioned previously, the contractile speed of both normal and dystrophic muscles changes relatively rapidly over this period of time, and a large error with respect to age (4 weeks * 3 days), as estimated by Bressler et al,5 could easily explain their results. Indeed, such an error may be associated with a bias in the sampling of dystrophic animals, by selecting older animals which, after all, would be more likely to express the characteristic features of the disease.…”

Section: Discussionmentioning

confidence: 89%

Effect of low Ca²⁺ solution on muscle contraction of developing, preclinical dystrophic (DY^2J) mice

Dangain

Neering

1992

Muscle and Nerve

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EDL muscles from normal and dystrophic (dy2j) mice aged 7 to 21 days of postnatal life were examined. Muscles were divided into 2 groups according to age, 7 to 14 days and 16 to 21 days postnatal, so as to assess age- and/or phenotype-related differences in the muscle response to low Ca2+ solution. Tension production was already much impaired in "predystrophic" muscles. At this stage, however, there was essentially no difference in twitch kinetics between normal and dystrophic muscles. Upon exposure to low Ca2+ solution, twitch responses of both normal and dystrophic muscles declined in a similar manner. In the youngest animals studied (7 to 14 days), the tetanic responses of both normal and dystrophic muscles to low Ca2+ solution were also similar. In animals 15 to 21 days old, however, the tetanic tension developed in low Ca2+ solution by dystrophic muscles, was significantly less than that of normal. Moreover, under these conditions (i.e., in low Ca2+ solution), and following tetanic stimulation, the membrane potential of dystrophic muscles in this age group was significantly more depolarized than that of normal muscles. Our results suggest that the ability of the cell to deal with extracellular Ca2+ is normal in predystrophic muscles up to 21 days of postnatal life. The results also clearly point to the fragility of the membrane in these muscles.

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Section: Discussionmentioning

confidence: 89%

Effect of low Ca²⁺ solution on muscle contraction of developing, preclinical dystrophic (DY^2J) mice

Dangain

Neering

1992

Muscle and Nerve

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“…It is clear, however, that this alteration of Ca 2+ signalling in mdx fibres is hidden when experiments are performed with 5 m m EGTA in internal solution since the kinetics of the transients from normal and mdx fibres are statistically similar under this condition (Table 1 and Figs 2 and 3). Whatever the cause, the prolongation of the decay phase of the AP‐evoked Ca 2+ transient of mdx fibres may explain the lengthening of the relaxation time of dystrophic muscle contraction (Parslow & Parry, 1981; Bressler et al 1983; Dangain & Vrbova, 1984).…”

Section: Discussionmentioning

confidence: 99%

The action potential‐evoked sarcoplasmic reticulum calcium release is impaired in mdx mouse muscle fibres

Woods

Novo

DiFranco

et al. 2004

The Journal of Physiology

104

161

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The mdx mouse, a model of the human disease Duchenne muscular dystrophy, has skeletal muscle fibres which display incompletely understood impaired contractile function. We explored the possibility that action potential-evoked Ca 2+ release is altered in mdx fibres. Action potential-evoked Ca 2+ -dependent fluorescence transients were recorded, using both low and high affinity Ca 2+ indicators, from enzymatically isolated fibres obtained from extensor digitorum longus (EDL) and flexor digitorum brevis (FDB) muscles of normal and mdx mice. Fibres were immobilized using either intracellular EGTA or N -benzyl-p-toluene sulphonamide, an inhibitor of the myosin II ATPase. We found that the amplitude of the action potential-evoked Ca 2+ transients was significantly decreased in mdx mice with no measured difference in that of the surface action potential. In addition, Ca 2+ transients recorded from mdx fibres in the absence of EGTA also displayed a marked prolongation of the slow decay phase. Model simulations of the action potential-evoked transients in the presence of high EGTA concentrations suggest that the reduction in the evoked sarcoplasmic reticulum Ca 2+ release flux is responsible for the decrease in the peak of the Ca 2+ transient in mdx fibres. Since the myoplasmic Ca 2+ concentration is a critical regulator of muscle contraction, these results may help to explain the weakness observed in skeletal muscle fibres from mdx mice and, possibly, Duchenne muscular dystrophy patients.

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“…Since then, fatigue free properties of dystrophic muscles have been reported by many workers (Eberstein and Sandow, 1963;Hinterbuchner et al, 1966;Hoekman, 1977). It has been also well known that muscle units are classified into at least three distinct types based upon fatigue sensitivity and SOL muscles are consisted of mainly slow conducting and fatigue resistant units (Burke et al, 1973;Hammarberg and Kellerth, 1975;Bressler et al, 1983). In spite of differences in the method between ours and those fatigue experiments, a similar conclusion was obtained; one could say that both dystrophic MG and SOL of various strains of mice are endowed with fatigue resistant properties.…”

Section: Resultsmentioning

confidence: 96%

“…Parslow and Parry (1981) also argued continuous activation of hind limb muscles in dystrophic mice as one possible cause of the fact that contractile properties of fasttwitch EDL of dystrophic mice were shifted toward those of slow-twitch muscles. Bressler et al (1983) pointed out that, in addition to postural changes of hind limbs induced by dystrophic processes, fiber composition of individual muscles was not well controlled in dystrophic mice. Thus, conclusive data have not yet been reported that indicate whether this shift reflects a cause or an effect of dystrophic processes.…”

Section: Discussionmentioning

confidence: 99%

Comparison of Fatigue Resistant Properties of Gastrocnemius and Soleus Muscles between Muscular Dystrophic Mice and Other Strains of Mice

Totsuka

Watanabe

Uramoto

et al. 1984

Congenital Anomalies

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Muscular potentials were recorded from medial gastrocnemius (MG) and soleus muscles (SOL) of dystrophic and normal mice of the strain C57BL/6J‐dy, dwarf and normal mice of the strain DW/J, and brachymorphic mice of the strain C57BL/6J‐Zwi. The mice were anesthetized with urethane and the sciatic nerve was stimulated at 0.5 and 5 Hz with square pulses. When the frequency of stimulation was raised from 0.5 to 5 Hz and maintained at the latter frequency for 10 min, muscular potentials of dystrophic MG decreased slightly, whereas the other MGs showed a rapid and remarkable reduction in amplitudes. In addition, muscular potentials of SOL of all mice were slightly potentiated. Thus, changing patterns of muscular potentials of dystrophic MG were shifted toward those characteristic of SOLs.

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Changes in isometric contractile properties of fast-twitch and slow-twitch skeletal muscle of dystrophic mice during postnatal development

Cited by 22 publications

References 25 publications

Effect of low Ca²⁺ solution on muscle contraction of developing, preclinical dystrophic (DY^2J) mice

Effect of low Ca²⁺ solution on muscle contraction of developing, preclinical dystrophic (DY^2J) mice

The action potential‐evoked sarcoplasmic reticulum calcium release is impaired in mdx mouse muscle fibres

Comparison of Fatigue Resistant Properties of Gastrocnemius and Soleus Muscles between Muscular Dystrophic Mice and Other Strains of Mice

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Changes in isometric contractile properties of fast-twitch and slow-twitch skeletal muscle of dystrophic mice during postnatal development

Cited by 22 publications

References 25 publications

Effect of low Ca2+ solution on muscle contraction of developing, preclinical dystrophic (DY2J) mice

Effect of low Ca2+ solution on muscle contraction of developing, preclinical dystrophic (DY2J) mice

The action potential‐evoked sarcoplasmic reticulum calcium release is impaired in mdx mouse muscle fibres

Comparison of Fatigue Resistant Properties of Gastrocnemius and Soleus Muscles between Muscular Dystrophic Mice and Other Strains of Mice

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Effect of low Ca²⁺ solution on muscle contraction of developing, preclinical dystrophic (DY^2J) mice

Effect of low Ca²⁺ solution on muscle contraction of developing, preclinical dystrophic (DY^2J) mice