Relationships between visual cycle retinoids, rhodopsin phosphorylation and phototransduction in mouse eyes during light and dark-adaptation

Phosphorylation and regeneration of rhodopsin, the prototypical G-Protein Coupled Receptor, each can influence light- and dark-adaptation. To evaluate their relative contributions we quantified rhodopsin, retinoids, phosphorylation and photosensitivity in mice during 90 minutes of illumination followed by dark-adaptation. During illumination, all-trans retinyl esters and, to a lesser extent, all-trans retinal, accumulate and reach steady state within an hour. Each major phosphorylation site on rhodopsin reaches a steady state level of phosphorylation at a different time during illumination. The dominant factor that limits dark adaptation is isomerisation of retinal. During dark adaptation dephosphorylation of rhodopsin occurs in two phases. The faster phase corresponds to rapid dephosphorylation of regenerated rhodopsin present at the end of the illumination period. The slower phase corresponds to dephosphorylation of rhodopsin as it forms by regeneration. We conclude that rhodopsin phosphorylation has three physiological functions, it quenches phototransduction, it reduces sensitivity during light-adaptation and it suppresses bleached rhodopsin activity during dark adaptation.