The Journal of Neurophysiology Vol. 82 No. 5 November 1999, pp. 2428-2440
Copyright ©1999 by the American Physiological Society

LVA and HVA Ca²⁺ Currents in Ventricular Muscle Cells of the Lymnaea Heart

 ¹Sussex Centre for Neuroscience, School of Biological Sciences, University of Sussex, Falmer, Brighton BN1 9QG; and  ²School of Pharmacy and Biomolecular Sciences, University of Brighton, Moulsecoomb, Brighton BN2 4GJ, United Kingdom

Yeoman, M. S., B. L. Brezden, and P. R. Benjamin. LVA and HVA Ca²⁺ Currents in Ventricular Muscle Cells of the Lymnaea Heart. J. Neurophysiol. 82: 2428-2440, 1999. The single-electrode voltage-clamp technique was used to characterize voltage-gated Ca²⁺ currents in dissociated Lymnaea heart ventricular cells. In the presence of 30 mM tetraethylammonium (TEA), two distinct Ca²⁺ currents could be identified. The first current activated between 70 and 60 mV. It was fully available for activation at potentials more negative than 80 mV. The current was fast to activate and inactivate. The inactivation of the current was voltage dependent. The current was larger when it was carried by Ca²⁺ compared with Ba²⁺, although changing the permeant ion had no observable effect on the kinetics of the evoked currents. The current was blocked by Co²⁺ and La³⁺ (1 mM) but was particularly sensitive to Ni²⁺ ions (50% block with 100 µM Ni²⁺) and insensitive to low doses of the dihydropyridine Ca²⁺ channel antagonist, nifedipine. All these properties classify this current as a member of the low-voltage-activated (LVA) T-type family of Ca²⁺ currents. The activation threshold of the current (70 mV) suggests that it has a role in pacemaking and action potential generation. Muscle contractions were first seen at 50 mV, indicating that this current might supply some of the Ca²⁺ necessary for excitation-contraction coupling. The second, a high-voltage-activated (HVA) current, activated at potentials between 40 and 30 mV and was fully available for activation at potentials more negative than 60 mV. This current was also fast to activate and with Ca²⁺ as the permeant ion, inactivated completely during the 200-ms voltage step. Substitution of Ba²⁺ for Ca²⁺ increased the amplitude of the current and significantly slowed the rate of inactivation. The inactivation of this current appeared to be current rather than voltage dependent. This current was blocked by Co²⁺ and La³⁺ ions (1 mM) but was sensitive to micromolar concentrations of nifedipine (50% block 10 µM nifedipine) that were ineffective at blocking the LVA current. These properties characterize this current as a L-type Ca²⁺ current. The voltage sensitivity of this current suggests that it is also important in generating the spontaneous action potentials, and in providing some of the Ca²⁺ necessary for excitation-contraction coupling. These data provide the first detailed description of the voltage-dependent Ca²⁺ currents present in the heart muscle cells of an invertebrate and indicate that pacemaking in the molluscan heart has some similarities with that of the mammalian heart.