Voltage-activated calcium currents from single, isolated turtle retinal ganglion cells were characterized with standard whole cell patch clamp techniques. Calcium current amplitude was increased with the use of 10 mM extracellular Ca2+, whereas sodium and potassium currents were pharmacologically suppressed. 2. A transient component, expressed in approximately 39% of the cells recorded from, closely resembled the T-type calcium current described previously in other tissues. This component activated at low voltages (around -50 mV from a holding potential of -70 mV) and inactivated with a time constant 10-30 ms at -20 mV; the inactivation was strongly voltage dependent. Substitution of Ca2+ with Ba2+ reduced this current in most cases or had no effect in some instances. Surprisingly, the transient calcium current was potentiated by Bay-K 8644 and inhibited by nifedipine in some of the ganglion cells tested. 3. A sustained component, which activated at between -20 and -10 mV from a holding potential of -70 mV, was found in all ganglion cells from which we recorded. This component was substantially larger when equimolar Ba2+ replaced Ca2+ as the charge carrier, and was sensitive to the dihydropyridine agonist Bay-K 8644 and the antagonist nifedipine. Thus the sustained current in turtle retinal ganglion cells was similar to the L-type calcium current described in chick DRG neurons. However, unlike the typical L-type current, this component in turtle ganglion cells showed an inactivation that was highly dependent on the intracellular free Ca2+ concentration but not the membrane potential. 4. Synthetic omega-conotoxin MVIIC selectively blocked the sustained calcium current while sparing the transient component. It could completely block the sustained current that was resistant to nifedipine in some cells. Thus there may exist several different high voltage-activated calcium channels in turtle retinal ganglion cells.
