Visual phototransduction

At rest, the photoreceptor cells are continually releasing glutamate at the synaptic terminal to maintain the potential.

The signal remains as a graded polarization in all cells until it reaches the RGCs, where it is converted to an action potential and transmitted to the brain.

In the first week after birth, cells mature and the eye becomes fully functional at the time of opening.

A high density of Na+-K+ pumps enables the photoreceptor to maintain a steady intracellular concentration of Na+ and K+.

When light intensity decreases, that is, in the dark environment, glutamate release by photoreceptors increases.

This dark current keeps the cell depolarized at about −40 mV, leading to glutamate release which inhibits excitation of neurons.

In the cone pathway, glutamate: In summary: Light closes cGMP-gated sodium channels, reducing the influx of both Na+ and Ca2+ ions.

During recovery (dark adaptation), the low Ca2+ levels induce recovery (termination of the phototransduction cascade), as follows: In more detail: GTPase Accelerating Protein (GAP) of RGS (regulators of G protein signaling) interacts with the alpha subunit of transducin, and causes it to hydrolyse its bound GTP to GDP, and thus halts the action of phosphodiesterase, stopping the transformation of cGMP to GMP.

It is this pathway, where Metarhodopsin II is phosphorylated and bound to arrestin and thus deactivated, which is thought to be responsible for the S2 component of dark adaptation.

When it absorbs a photon, 11-cis-retinal undergoes photoisomerization to all-trans-retinal, which changes the conformation of the opsin GPCR leading to signal transduction cascades which causes closure of cyclic GMP-gated cation channel, and hyperpolarization of the photoreceptor cell.

Following photoisomerization, all-trans-retinal is released from the opsin protein and reduced to all-trans-retinol, which travels to the retinal pigment epithelium to be "recharged".

[8] Finally, it is oxidized to 11-cis-retinal before traveling back to the photoreceptor cell outer segment where it is again conjugated to an opsin to form new, functional visual pigment (retinylidene protein), namely photopsin or rhodopsin.

[citation needed] Invertebrate photoreceptor cells differ morphologically and physiologically from their vertebrate counterparts.

Visual stimulation in vertebrates causes a hyperpolarization (weakening) of the photoreceptor membrane potential, whereas invertebrates experience a depolarization with light intensity.

Single-photon events produced under identical conditions in invertebrates differ from vertebrates in time course and size.

Representation of molecular steps in photoactivation (modified from Leskov et al., 2000 [ 4 ] ). Depicted is an outer membrane disk in a rod. Step 1 : Incident photon (hν) is absorbed and activates a rhodopsin (likewise photopsin ) by conformational change in the disk membrane to R*. Step 2 : Next, R* makes repeated contacts with transducin molecules, catalyzing its activation to G* by the release of bound GDP in exchange for cytoplasmic GTP, which expels its β and γ subunits. Step 3 : G* binds inhibitory γ subunits of the phosphodiesterase (PDE) activating its α and β subunits. Step 4 : Activated PDE hydrolyzes cGMP. Step 5 : Guanylyl cyclase (GC) synthesizes cGMP, the second messenger in the phototransduction cascade. Reduced levels of cytosolic cGMP cause cyclic nucleotide gated channels to close preventing further influx of Na + and Ca 2+ .
The absorption of light leads to an isomeric change in the retinal molecule.