Visual phototransduction is a process that involves the conversion of light into electrical signals within the retina, which are then processed and sent to the brain. The photoreceptor retinal cells involved in phototransduction are rods and cones. Structurally, rods and cones are made up of an outer segment that contain the visual pigment and an inner segment that makes synaptic contact with bipolar and horizontal cells of the retina. The outer segment of rods and cones are involved in phototransduction.Light absorbed by the outer segment results in the closure of cationic channels, which in turn cause hyperpolarization. The hyperpolarization in the photoreceptor cell is relayed to the synaptic terminals, where the release of neurotransmitter is slowed down. The molecular events involved from light absorption to channel closure are as follows.
At the center of phototransduction is the visual protein Rhodopsin, which is comprised of the membrane protein Opsin bound to the chromophore 11-cis-retinal. When Rhodopsin absorbs a photon of light, 11-cis-retinal isomerizes to all trans retinal, resulting in the cytoplasmic face of opsin becoming catalytically active. All-trans-retinal dissociates from opsin at this stage, to be regenerated as 11-cis-retinal in the retinal pigment epithelium. Activated Opsin triggers the trimeric G protein Transducin, resulting in the exchange of GDP for GTP on its αsubunit. At this stage the signal is greatly amplified, with a single activated Opsin triggering the generation of hundreds of activated Transducin moieties. Transducin-GTP goes on to activate a third protein, cGMP phosphodiesterase (PDE) which hydrolyzes cGMP to 5'-GMP. The low concentration of cGMP results in the closure of cationic channels, leading to the hyperpolarization of the photoreceptor cell and decreased release of neurotransmitters at the synapse. cGMP, whose levels are enhanced in the absence of light, allows opening of cationic channels resulting in depolarization of the photoreceptor cell. Depolarization causes further formation of cGMP via activation of Guanylate cyclase (GC).
Quenching of the light response of retinal rods and cones requires the inactivation of Opsin by Arrestin and Rhodopsin kinase. Additionally, the response to light can be quenched by the GTP hydrolysis of Transducin-GTP catalyzed by a protein complex that includes regulator of G-protein signaling -RGS9.
This pathway highlights the important molecular events in phototransduction within the outer segments of rod and cone cells.