D. Ursu et al., Excitation-contraction coupling in skeletal muscle of a mouse lacking the dihydropyridine receptor subunit gamma 1, J PHYSL LON, 533(2), 2001, pp. 367-377
1. In skeletal muscle, dihydropyridine (DHP) receptors control both Ca2+ en
try (L-type current) and internal Ca2+ release in a voltage-dependent manne
r. Here we investigated the question of whether elimination of the skeletal
muscle-specific DHP receptor subunit gamma1 affects excitation-contraction
(E-C) coupling. We studied intracellular Ca2+ release and force production
in muscle preparations of a mouse deficient in the gamma1 subunit (gamma-/
-).
2. The rate of internal Ca2+ release at large depolarization (+20 mV) was d
etermined in voltage-clamped primary-cultured myotubes derived from satelli
te cells of adult mice by analysing fura-2 fluorescence signals and estimat
ing the concentration of free and bound Ca2+. On average, gamma-/- cells sh
owed an increase in release of about one-third of the control value and no
alterations in the time course
3. Voltage of half-maximal activation (V-1/2) and voltage sensitivity (k) w
ere not significantly different in gamma-/- myotubes, either for internal C
a2+ release activation or for the simultaneously measured L-type Ca2+ condu
ctance. The same was true for maximal Ca2+ inward current and conductance.
4. Contractions evoked by electrical stimuli were recorded in isolated exte
nsor digitorum longus (EDL; fast, glycolytic) and soleus (slow, oxidative)
muscles under normal conditions and during fatigue induced by repetitive te
tanic stimulation. Neither time course nor amplitudes of twitches and tetan
i nor force-frequency relations showed significant alterations in the gamma
1-deficient muscles.
5. In conclusion, the overall results show that the gamma1 subunit is not e
ssential for voltage-controlled Ca2+ release and force production.