Retinal ganglion cells (RGCs) consolidate visual processing and constitute the last step prior to the transmission of signals to higher brain centers. RGC death is a major cause of visual impairment in optic neuropathies, including glaucoma, age‑related macular degeneration, diabetic retinopathy, uveoretinitis and vitreoretinopathy. Discharge patterns of RGCs are primarily determined by the presence of ion channels. As the most diverse group of ion channels, potassium (K+) channels play key roles in modulating the electrical properties of RGCs. Biochemical, molecular and pharmacological studies have identified a number of K+ channels in RGCs, including inwardly rectifying K+ (Kir), ATP‑sensitive K+ (KATP), tandem‑pore domain K+ (TASK), voltage‑gated K+ (Kv), ether‑à‑go‑go (Eag) and Ca2+‑activated K+ (KCa) channels. Kir channels are important in the maintenance of the resting membrane potential and controlling RGC excitability. KATP channels are involved in RGC survival and neuroprotection. TASK channels are hypothesized to contribute to the regulation of resting membrane potentials and firing patterns of RGCs. Kv channels are important regulators of cellular excitability, functioning to modulate the amplitude, duration and frequency of action potentials and subthreshold depolarizations, and are also important in RGC development and protection. Eag channels may contribute to dendritic repolarization during excitatory postsynaptic potentials and to the attenuation of the back propagation of action potentials. KCa channels have been observed to contribute to repetitive firing in RGCs. Considering these important roles of K+ channels in RGCs, the study of K+ channels may be beneficial in elucidating the pathophysiology of RGCs and exploring novel RGC protection strategies.