The GPCR signaling cascade in the retinal photoreceptor cells, rods and cones, provides high signal amplification and allows rods to respond reliably to single photons. At the same time, rods remain operational under light fluxes up to 105 photons per second, which is supported by a highly efficient system of light adaptation. Light adaptation is based on negative feedback chains, mainly through changes in the intracellular concentration of Ca2+ ions. There are three reliably identified loops of calcium regulation – the acceleration of quenching of photoactivated rhodopsin, the acceleration of cGMP synthesis by guanylate cyclase, and an increase of cGMP-controlled ion channels’ affinity to the nucleotide. However, it is known that there are additional one or two highly effective adaptation mechanisms, one of which regulates the lifetime of activated phosphodiesterase; for the second one, the target of regulation is unknown. The messengers of these regulations also remain unknown. While studying these mechanisms, we discovered a new phenomenon that was not noticed in previous works. We found that the restoration of rod’s dark current after turning off the non-saturating adapting light can take 20-30 s. Moreover, after the membrane current formally returns to the dark level, the sensitivity of the cell to testing stimuli remains reduced for one to two minutes. We called this phenomenon “adaptation memory”. Adaptation memory resembles the phenomenology of the afterimages. The gradual return of the membrane current to the dark level could correspond to the fading of positive afterimage. Long-term decrease in the sensitivity of photoreceptors to an additional stimulation can create a negative afterimage. As far as we know, this is the first experimental physiological demonstration of the possibility of afterimages generation already at the level of single photoreceptors.