In situ study of the sarcoplasmic reticulum function in control and <i>mdx</i> mouse diaphragm muscle

Khammari, A; Péréon, Y; Baudet, S; Noireaud, J

doi:10.1139/y98-122

Cited by 8 publications

(7 citation statements)

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“…Our finding of normal Ca 2ϩ -ATPase activity in mechanically skinned T-tubule sealed fibers is in agreement with a previous report of SR Ca 2ϩ -handling in cooling contracture experiments on bundles of diaphragm muscle fibers from mdx mice (16). These results differ from another study by Kargacin and Kargacin (15), who reported decreased SR Ca 2ϩ -ATPase activity in reconstituted SR membrane vesicles prepared from muscles of mdx compared with control mice.…”

Section: Discussionsupporting

confidence: 90%

“…Previous studies have determined that the sensitivity to caffeine is greater in slow than fast muscle fibers, most likely due to the level of saturation of SR Ca 2ϩ loading (9). In our experiments we found no differences in SR Ca 2ϩ loading or Ca 2ϩ leak in EDL muscle fibers from mdx and control mice and assumed an identical SR Ca 2ϩ content in the fibers (16). Further experiments comparing the saturation of SR Ca 2ϩ loading between fibers from mdx and control mice are warranted.…”

Section: Discussionsupporting

confidence: 61%

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Depolarization-induced contraction and SR function in mechanically skinned muscle fibers from dystrophic mdx mice

Plant

Lynch

2003

American Journal of Physiology-Cell Physiology

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Dystrophin is absent in muscle fibers of patients with Duchenne muscular dystrophy (DMD) and in muscle fibers from the mdx mouse, an animal model of DMD. Disrupted excitation-contraction (E-C) coupling has been postulated to be a functional consequence of the lack of dystrophin, although the evidence for this is not entirely clear. We used mechanically skinned fibers (with a sealed transverse tubular system) prepared from fast extensor digitorum longus muscles of wild-type control and dystrophic mdx mice to test the hypothesis that dystrophin deficiency would affect the depolarization-induced contractile response (DICR) and sarcoplasmic reticulum (SR) function. DICR was similar in muscle fibers from mdx and control mice, indicating normal voltage regulation of Ca2+ release. Nevertheless, rundown of DICR (<50% of initial) was reached more rapidly in fibers from mdx than control mice [control: 32 ± 5 depolarizations ( n = 14 fibers) vs. mdx: 18 ± 1 depolarizations ( n = 7) before rundown, P < 0.05]. The repriming rate for DICRs was decreased in fibers from mdx mice, with lower submaximal DICR observed after 5, 10, and 20 s of repriming compared with fibers from control mice ( P < 0.05). SR Ca2+ reloading was not different in fibers from control and mdx mice, and no difference was observed in SR Ca2+ leak. Caffeine (2–7 mM)-induced contraction was diminished in fibers from mdx mice compared with control ( P < 0.05), indicating depressed SR Ca2+ release channel activity. Our findings indicate that fast fibers from mdx mice exhibit some impairment in the events mediating E-C coupling and SR Ca2+ release channel activity.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 61%

Depolarization-induced contraction and SR function in mechanically skinned muscle fibers from dystrophic mdx mice

Plant

Lynch

2003

American Journal of Physiology-Cell Physiology

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“…However, the high activity of calcium‐activated potassium channels, as established by cell‐attached patch clamp recordings on freshly dissociated muscle fibres, is clear functional evidence in favour of a basal subsarcolemmal increase of calcium ions ( Mallouk et al ., 2000 ). Similarly, some controversies have been found when the time course of calcium transients has been evaluated, since some authors reported no change while others showed a longer decay time of the transient ( Khammari et al ., 1998 ; Tutdibi et al ., 1999 ; Collet et al ., 1999 ). This latter event can result from a decreased activity of calcium ATPase pump of sarcoplasmic reticulum (SR) for the impairment of energy products, due to calcium overload in mitochondria ( Pulido et al ., 1998 ; Kargacin & Kargacin, 1996 ; Rüegg & Gillis, 1999 ).…”

Section: Introductionmentioning

confidence: 99%

Alteration of excitation‐contraction coupling mechanism in extensor digitorum longus muscle fibres of dystrophic mdx mouse and potential efficacy of taurine

Luca

Pierno

Liantonio

et al. 2001

British J Pharmacology

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1 No clear data is available about functional alterations in the calcium-dependent excitationcontraction (e-c) coupling mechanism of dystrophin-de®cient muscle of mdx mice. 2 By means of the intracellular microelectrode`point' voltage clamp method, we measured the voltage threshold for contraction (mechanical threshold; MT) in intact extensor digitorum longus (EDL) muscle ®bres of dystrophic mdx mouse of two di erent ages: 8 ± 12 weeks, during the active regeneration of hind limb muscles, and 6 ± 8 months, when regeneration is complete. 3 The EDL muscle ®bres of 8 ± 12-week-old wildtype animals had a more negative rheobase voltage (potential of equilibrium for contraction-and relaxation-related calcium movements) with respect to control mice of 6 ± 8 months. However, at both ages, the EDL muscle ®bres of mdx mice contracted at more negative potentials with respect to age-matched controls and had markedly slower time constants to reach the rheobase. 4 The in vitro application of 60 mM taurine, whose normally high intracellular muscle levels play a role in e-c coupling, was without e ect on 6 ± 8-month-old wildtype EDL muscle, while it signi®cantly ameliorated the MT of mdx mouse. 5 HPLC determination of taurine content at 6 ± 8 months showed a signi®cant 140% rise of plasma taurine levels and a clear trend toward a decrease in amino acid levels in hind limb muscles, brain and heart, suggesting a tissue di culty in retaining appropriate levels of the amino acid. 6 The data is consistent with a permanent alteration of e-c coupling in mdx EDL muscle ®bres. The alteration could be related to the proposed increase in intracellular calcium, and can be ameliorated by taurine, suggesting a potential therapeutic role of the amino acid.

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“…On the other hand, studies at the single-fiber level revealed that EDL and soleus muscles of mdx mice are affected differently by the absence of dystrophin (13,29). The different dysfunction of the mdx dystrophic muscles has been correlated with changes of myosin heavy-chain (MHC) composition and enzymatic kinetic of myofibrillar proteins Ca 2ϩ -sensitivity as well as of excitation-contraction coupling (1,12,13,28,35,41,43).…”

mentioning

confidence: 99%

Deficiency of α-sarcoglycan differently affects fast- and slow-twitch skeletal muscles

Danieli-Betto¹,

Esposito²,

Germinario³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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Alpha-sarcoglycan (Sgca) is a transmembrane glycoprotein of the dystrophin complex located at skeletal and cardiac muscle sarcolemma. Defects in the alpha-sarcoglycan gene (Sgca) cause the severe human-type 2D limb girdle muscular dystrophy. Because Sgca-null mice develop progressive muscular dystrophy similar to human disorder they are a valuable animal model for investigating the physiopathology of the disorder. In this study, biochemical and functional properties of fast-twitch extensor digitorum longus (EDL) and slow-twitch soleus muscles of the Sgca-null mice were analyzed. EDL muscle of Sgca-null mice showed twitch and tetanic kinetics comparable with those of wild-type controls. In contrast, soleus muscle showed reduction of twitch half-relaxation time, prolongation of tetanic half-relaxation time, and increase of maximal rate of rise of tetanus. EDL muscle of Sgca-null mice demonstrated a marked reduction of specific twitch and tetanic tensions and a higher resistance to fatigue compared with controls, changes that were not evident in dystrophic soleus. Contrary to EDL fibers, soleus muscle fibers of Sgca-null mice distinctively showed right shift of the pCa-tension (pCa is the negative log of Ca2+ concentration) relationships and reduced sensitivity to caffeine of sarcoplasmic reticulum. Both EDL and soleus muscles showed striking changes in myosin heavy-chain (MHC) isoform composition, whereas EDL showed a larger number of hybrid fibers than soleus. In contrast to the EDL, soleus muscle of Sgca-null mice contained a higher number of regenerating fibers and thus higher levels of embryonic MHC. In conclusion, this study revealed profound distinctive biochemical and physiological modifications in fast- and slow-twitch muscles resulting from alpha-sarcoglycan deficiency.

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In situ study of the sarcoplasmic reticulum function in control and mdx mouse diaphragm muscle

Cited by 8 publications

References 0 publications

Depolarization-induced contraction and SR function in mechanically skinned muscle fibers from dystrophic mdx mice

Depolarization-induced contraction and SR function in mechanically skinned muscle fibers from dystrophic mdx mice

Alteration of excitation‐contraction coupling mechanism in extensor digitorum longus muscle fibres of dystrophic mdx mouse and potential efficacy of taurine

Deficiency of α-sarcoglycan differently affects fast- and slow-twitch skeletal muscles

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