The photoreceptors and bipolar cells in the vertebrate retina were considered non-spiking neurons. However, we showed that human photoreceptors can generate sodium action potentials in response to membrane depolarization (Kawai et al, 2001). In this study, we performed physiological and molecular biological analyses to confirm the presence of the sodium channel in photoreceptors and bipolar cell in the human retina. A small piece of retina was excised from each of 15 adult patients with a fresh retinal detachment during the surgical procedure to reattach the retina. In the standard vitreous surgery to reattach a detached retina, the fluid between the detached retina and the retinal pigment epithelium is removed through an artificial retinal hole that is made during surgery. To make the artificial hole, a small piece of retina (diameter 1 mm) had to be exercised, and this piece was used in our experiment. The estimated time between retinal detachment and surgery was 2 days. In all cases, functional recovery of the retina occurred after surgery, indicating that there was no severe pathology of the retina. All experiments were performed in compliance with the guideline of the Declaration of Helsinki and the ethics committee of Fujita Health University. All patients were informed of the purpose of the surgery and the necessity of removing the retinal tissue, and signed informed consent to allow the use of the tissue for these experiments. The SCN2A, the type II sodium channel (Nav1.2) transcript, was observed in photoreceptors and bipolar cells by single-cell RT-PCR analysis. Under voltage-clamp conditions, depolarizing voltage steps induced fast transient inward currents, which were inactivated within 5 ms and blocked by a voltage-gated sodium channel blocker tetrodotoxin, in several bipolar cells, as well as rods and cones. These results indicate that human photoreceptors and bipolar cells express Nav1.2 voltage-gated sodium channels, and suggest that the sodium channels may serve to amplify the release of the neurotransmitter when membrane potential is depolarized. We also observed the hyperpolarization-activated current, the h current (Ih), in human rods. Dopamine reversibly decreased the amplitude of the Ih induced by hyperpolarizing voltage steps. The D2 dopamine agonist inhibited Ih, but the D1 agonist had no effect. Dopamine-induced reduction of Ih amplitude was blocked by the D2 dopamine antagonist. These results suggest that dopamine reduced Ih through a D2 receptor and that dopamine slows the recovery phase of responses to light stimuli by inhibiting Ih in human rods. We consider that Ih may contribute to preventing visual flickering by inhibiting the generation of spontaneous Na+ spikes in human photoreceptors.