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Additional recommended knowledge
The process of phototransduction is a complicated one, and in order to understand it, one must have an understanding of the structure of the photoreceptor cells in the eye: the rods and cones. These cells contain a chromophore (11-cis-retinal, the aldehyde of Vitamin A1 and light-absorbing portion) bound to a cell membrane protein, opsin. Rods deal with low light level and do not mediate colour vision. Cones, on the other hand, can code the colour of an image through comparison of the outputs of the three different types of cones. Each cone type responds best to certain wavelengths, or colours, of light because each type has a slightly different opsin. The three types of cones are L-cones, M-cones and S-cones that respond optimally to long wavelengths (reddish colour), medium wavelengths (greenish colour), and short wavelengths (bluish colour) respectively.
To understand the photoreceptor's behaviour to light intensities, it is necessary to understand the roles of different currents.
There is an ongoing outward potassium current through nongated K+-selective channels. This outward current tends to hyperpolarise the photoreceptor at around -70 mV (the equilibrium potential for K+).
There is also an inward sodium current carried by cGMP-gated sodium channels. This so-called 'dark current' depolarises the cell to around -40 mV. Note that this is significantly more depolarised than most other neurons.
A high density of Na+-K+ pumps enables the photoreceptor to maintain a steady intracellular concentration of Na+ and K+.
In the dark
Photoreceptor cells are strange cells because they are depolarised in the dark, i.e. light hyperpolarises and switches off these cells, and it is this 'switching off' that activates the next cell and sends an excitatory signal down the neural pathway.
In the dark, cGMP levels are high and keep cGMP-gated sodium channels open allowing a steady inward current, called the dark current. This dark current keeps the cell depolarised at about -40 mV.
The depolarisation of the cell membrane opens voltage-gated calcium channels. An increased intracellular concentration of Ca+ causes vesicles containing special chemicals, called neurotransmitters, to merge with the cell membrane, therefore releasing the neurotransmitter into the synaptic cleft, an area between the end of one cell and the beginning of another neuron. The neurotransmitter released is glutamate, an excitatory neurotransmitter.
In the cone pathway glutamate:
In the light
Deactivation of the phototransduction cascade
GTPase Activating Protein (GAP) 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.
Guanylate Cyclase Activating Protein (GCAP) is a calcium binding protein, and as the calcium levels in the cell have decreased, GCAP dissociates from its bound calcium ions, and interacts with Guanylate Cyclase, activating it. Guanylate Cyclase then proceeds to transform GTP to cGMP, replenishing the cell's cGMP levels and thus reopening the sodium channels that were closed during phototransduction.
Finally, Metarhodopsin II is deactivated. Recoverin, another calcium binding protein, is normally bound to Rhodopsin Kinase when calcium is present. When the calcium levels fall during phototransduction, the calcium dissociates from recoverin, and rhodopsin kinase is released, when it proceeds to phosphorylate metarhodopsin II, which decreases its affinity for transducin. Finally, arrestin, another protein, binds the phosphorylated metarhodopsin II, completely deactivating it. Thus, finally, phototransduction is deactivated, and the dark current and glutamate release is restored. 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. The S2 component represents a linear section of the dark adaptation function present at the beginning of dark adaptation for all bleaching intensities.
All-trans retinal is transported to the pigment epithelial cells to be reduced to all-trans retinol, the precursor to 11-cis retinal. This is then transported back to the rods. All-trans retinol cannot be synthesised by humans and must be supplied by vitamin A in the diet. Deficiency of all-trans retinol can lead to night blindness. This is part of the bleach and recycle process of retinoids in the photoreceptors and retinal pigment epithelium.
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Visual_phototransduction". A list of authors is available in Wikipedia.|