In spiking neurons, phasic, calcium-dependent transmitter release is initiated when a presynaptic action potential activates voltage-dependent calcium channels. Vertebrate photoreceptors are nonspiking neurons that continuously release transmitter. This study uses patch-clamp recording to examine the electrophysiological properties of mammalian cones in intact retina. The cell capacitance was 10 ± 1 pF and the input resistance was 0.52 ± 0.46 G-ohms at −65 mV (31 cells). A specific membrane capacitance of 1.2 pF/cm2 was calculated. The cones did not appear to be chemically or electrically coupled. The calcium conductance averaged 3 ± 1 nS (five cells). Fifty percent of the calcium channels were active at −40 mV, and at this voltage the number of active channels changed e-fold for a 6-mV voltage change. At 25°C, the current reached a peak within about 1 ms after onset of a step to −35 mV. The calcium influx produced by depolarization activated a chloride conductance with a delay of a few milliseconds. The channels did not completely inactivate during maintained depolarization. The calcium channels were partially blocked by high concentrations of nifedipine, an L-type specific antagonist, and were recognized by an antibody raised against the L-type subunit α-1D. The immunohistochemical staining shows that the calcium channels are localized to the synaptic terminals. The immunohistochemical, physiological, and pharmacological properties indicate that the calcium channels in mammalian photoreceptors may represent a novel isoform, possibly with some homologies to the L-type class. The activation range of the channels matches the physiological operating range of photoreceptors.