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.