Recent reports on rod photoreceptor neuroprotection by Ca²⁺ channel blockers have pointed out the need to assess the effect of these blockers on mammalian rods. However, in mammals, rod electrophysiological characterization has been hampered by the small size of these photoreceptors which were instead extensively studied in non-mammalian vertebrates. To further characterize ionic conductances and to assess the pharmacology of Ca²⁺ channels in mammalian rods, freshly dissociated pig rod photoreceptors were recorded with the wholecell patch-clamp technique. Rod cells expressed: (1) a hyperpolarization-activated inwardrectifying conductance [I_h] sensitive to external Cs⁺, (2) a sustained outward K⁺ current [I_K] sensitive to tetraethylammonium, (3) a sustained voltage-gated Ca²⁺ current [I_Ca] sensitive to benzothiazepine (diltiazem) and phenylalkylamine (verapamil) derivatives, (4) a Ca²⁺- activated Cl^- current [I_Cl(Ca)], (5) a plasma membrane Ca²⁺-ATPase. The Ca²⁺ current showed a range of activation from positive potentials to -60 mV with a maximum between -30 and -20 mV. By contrast to other L-type Ca²⁺ channels, rod Ca²⁺ channels were blocked at similar and relatively high concentrations by the diltiazem isomers and verapamil. The biphasic dose-response for D-diltiazem confirmed the low sensitivity of Ca²⁺ channels for the molecule. The ATPase, which was localized at the axon terminal, was found to contribute to Ca²⁺ extrusion. These results suggest that the electrophysiological features of rod photoreceptors had been preserved during evolution from non-mammalian vertebrates to mammals. This work indicates further that mammalian rods express non classic L-type Ca²⁺ channels showing a low sensitivity to the diltiazem isomers used in neuroprotective studies.