LVA and HVA Ca2+ currents in ventricular muscle cells of the Lymnaea heart

LVA and HVA Ca2+ currents in ventricular muscle cells of the Lymnaea heart. J. Neurophysiol. 82: 2428-2440, 1999. The single-electrode voltage-clamp t echnique was used to characterize voltage-gated Ca2+ currents in dissociate d Lymnaea heart ventricular cells. In the presence of 30 mM tetraethylammon ium (TEA), two distinct Ca2+ currents could be identified. The first curren t activated between -70 and -60 mV. It was fully available for activation a t potentials more negative than -80 mV. The current was fast to activate an d inactivate. The inactivation of the current was voltage dependent. The cu rrent was larger when it was carried by Ca2+ compared with Ba2+, although c hanging the permeant ion had no observable effect on the kinetics of the ev oked currents. The current was blocked by Co2+ and La3+ (1 mM) but was part icularly sensitive to Ni2+ ions (approximate to 50% block with 100 mu M Ni2 +) and insensitive to low doses of the dihydropyridine Ca2+ channel antagon ist, nifedipine. All these properties classify this current as a member of the low-voltage-activated (LVA) T-type family of Ca2+ currents. The activat ion threshold of the current (-70 mV) suggests that it has a role in pacema king and action potential generation. Muscle contractions were first seen a t -50 mV, indicating that this current might supply some of the Ca2+ necess ary far excitation-contraction coupling. The second, a high-voltage-activat ed (HVA) current, activated at potentials between -40 and -30 mV and was fu lly available for activation at potentials more negative than -60 mV. This current was also fast to activate and with Ca2+ as the permeant ion, inacti vated completely during the 200-ms voltage step. Substitution of Ba2+ for C a2+ increased the amplitude of the current and significantly slowed the rat e of inactivation. The inactivation of this current appeared to be current rather than voltage dependent. This current was blocked by Co2+ and La3+ io ns (1 mM) but was sensitive to micromolar concentrations of nifedipine (app roximate to 50% block 10 mu M nifedipine) that were ineffective at blocking the LVA current. These properties characterize this current as a L-type Ca 2+ current. The voltage sensitivity of this current suggests that it is als o important in generating the spontaneous action potentials, and in providi ng some of the Ca2+ necessary for excitation-contraction coupling. These da ta provide the first detailed description of the voltage-dependent Ca2+ cur rents present in the heart muscle cells of an invertebrate and indicate tha t pacemaking in the molluscan heart has some similarities with that of the mammalian heart.