Expression of the alpha(2)delta subunit interferes with prepulse facilitation in cardiac L-type calcium channefs

We investigated the role of the accessory alpha(2)delta subunit on the volt age-dependent facilitation of cardiac L-type Ca2+ channels (alpha(1C)). alp ha(1C) Channels were coexpressed in Xenopus oocytes with beta(3) and alpha( 2)delta calcium channel subunits. In alpha(1C) + beta(3), the amplitude of the ionic current (measured during pulses to 10 mV) was in average similar to 1.9-fold larger after the application of a 200-ms prepulse to +80 mV. Th is phenomenon, commonly referred to as voltage-dependent facilitation, was not observed when alpha(2)delta was coexpressed with alpha(1C) + beta(3). I n alpha(1C) + beta(3), the prepulse produced a left shift (similar to 40 mV ) of the activation curve. Instead, the activation curve for alpha(1C) + be ta(3) + alpha(2)delta was minimally affected by the prepulse and had a volt age dependence very similar to the G-V curve of the alpha(1C) + beta(3) cha nnel facilitated by the prepulse. Coexpression of alpha(2)delta with alpha( 1C) + beta(3) seems to mimic the prepulse effect by shifting the activation curve toward more negative potentials, leaving little room for facilitatio n. The facilitation of alpha(1C) + beta(3) was associated with an increase of the charge movement. In the presence of alpha(2)delta, the charge remain ed unaffected after the prepulse. Coexpression of alpha(2)delta seems to se t all the channels in a conformational state from where the open state can be easily reached, even without prepulse.