Human retina contains two types of photoreceptors. Rods are very sensitive and enable vision in dim light conditions, whereas cones mediate daylight vision and color detection. In photoreceptors, absorption of photons causes conformational change and activation of visual pigment rhodopsin which in turn activates signalling cascade that leads to biochemical, electric and secretory cell response. The first step in phototransduction is activation of signalling G-protein transducin which activates phosphodiesterase. The later hydrolyses cyclic guanosine monophosphate (cGMP) thus lowering its concentration and decreasing open probability of cGMP-gated channels. In darkness, Na+ and Ca2+ ions enter the photoreceptor through cGMP-gated channels maintaining membrane potential at approximately –40 mV. Due to decreased cGMP these channels close, lowering the cytosolic cation concentration. Simmultaneously, the ionic fluxes through other channels and exchangers remain unaffected. This leads to photoreceptor hyperpolarisation which is electrotonically conducted to the synaptic terminal causing closure of voltage dependent Ca2+ channels and decrease in the exocytosis of neurotransmitter glutamate. After having responded to a light stimulus, the activated components of the phototransduction cascade have to return to their ground state, which is achieved through two mechanisms. The first mechanism enables deactivation and degradation of the activated rhodopsin, whereas the second mechanism deactivates complexes of activated transducin α-subunit and phosphodiesterase. Simmultaneously, cytoplasmic enzyme guanylyl cyclase is synthesizing cGMP thus restoring its basal concentration. Photoreceptors adapt to prolonged illumination by modulating the activity of guanyly cyclase and rhodopsin kinase as well as by changing sensitivity of cGMP-gated channels and bleaching of photopigments. All these effects are mediated by changes in intracellular Ca2+ concentration.