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Excitation‐contraction coupling in skeletal muscle of a mouse lacking the dihydropyridine receptor subunit γ1
Author(s) -
Ursu D.,
Sebille S.,
Dietze B.,
Freise D.,
Flockerzi V.,
Melzer W.
Publication year - 2001
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2001.0367a.x
Subject(s) - skeletal muscle , ryanodine receptor , biophysics , depolarization , chemistry , stimulation , myogenesis , dihydropyridine , contraction (grammar) , soleus muscle , medicine , endocrinology , intracellular , calcium , biology , biochemistry , organic chemistry
In skeletal muscle, dihydropyridine (DHP) receptors control both Ca 2+ entry (L‐type current) and internal Ca 2+ release in a voltage‐dependent manner. Here we investigated the question of whether elimination of the skeletal muscle‐specific DHP receptor subunit γ1 affects excitation‐contraction (E–C) coupling. We studied intracellular Ca 2+ release and force production in muscle preparations of a mouse deficient in the γ1 subunit (γ‐/‐). The rate of internal Ca 2+ release at large depolarization (+20 mV) was determined in voltage‐clamped primary‐cultured myotubes derived from satellite cells of adult mice by analysing fura‐2 fluorescence signals and estimating the concentration of free and bound Ca 2+ . On average, γ‐/‐ cells showed an increase in release of about one‐third of the control value and no alterations in the time course. Voltage of half‐maximal activation ( V 1/2 ) and voltage sensitivity ( k ) were not significantly different in γ‐/‐ myotubes, either for internal Ca 2+ release activation or for the simultaneously measured L‐type Ca 2+ conductance. The same was true for maximal Ca 2+ inward current and conductance. Contractions evoked by electrical stimuli were recorded in isolated extensor digitorum longus (EDL; fast, glycolytic) and soleus (slow, oxidative) muscles under normal conditions and during fatigue induced by repetitive tetanic stimulation. Neither time course nor amplitudes of twitches and tetani nor force‐frequency relations showed significant alterations in the γ1‐deficient muscles. In conclusion, the overall results show that the γ1 subunit is not essential for voltage‐controlled Ca 2+ release and force production.