The skeletal muscle L-type calcium channel or dihydropyridine receptor (DHPR) plays an integral role in excitation-contraction (e-c) coupling. Its activation initiates three sequential events: charge movement (Qr), calcium release, and calcium current (I_Ca-L). This relationship suggests that changes in Qr might affect release and I_Ca-L. Here we studied the effect of gabapentin on the three events generated by DHPRs in skeletal myotubes in culture. Gabapentin specifically binds to the 2/1 subunit of the brain and skeletal muscle DHPR. Myotubes were stimulated with a protocol which included a depolarizing prepulse to inactivate voltage-dependent proteins other than DHPRs. Gabapentin (50 µM) significantly increased Qr while decreasing the rate of rise of calcium transients. Gabapentin also reduced the maximum amplitude of the I_Ca-L (as we previously reported), without modifying the kinetics of activation. Exposure of gabapentin-treated myotubes to 10 µM nifedipine prevented the increase of Qr promoted by this drug, indicating that the extra charge recorded originated from DHPRs. Our data suggest that gabapentin dissociates the functions of the DHPR from the initial voltage-sensing step and implicates a role for the 2/ subunit in e-c coupling.