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Visual phototransduction is a process by which light is converted into electrical signals in the rod cells, cone cells and photosensitive ganglion cells of the retina of the eye.


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 (blueish 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:

  • Hyperpolarizes on-center bipolar cells. Glutamate that is released from the photoreceptors in the dark binds to metabotropic glutamate receptors (mGluR6), which, through a G-protein coupling mechanism, causes non-specific cation channels in the cells to close, thus hyperpolarizing the bipolar cell.
  • Depolarizes off-center bipolar cells. Binding of glutamate to ionotropic glutamate receptors results in an inward cation current that depolarizes the bipolar cell.

In the light

  1. A light photon interacts with the retinal in a photoreceptor. The retinal undergoes isomerisation, changing from the 11-cis to all-trans configuration.
  2. Retinal no longer fits into the opsin binding site.
  3. Opsin therefore undergoes a conformational change to metarhodopsin II.
  4. Metarhodopsin II is unstable and splits, yielding opsin and all-trans retinal.
  5. The opsin activates the regulatory protein transducin.
  6. Transducin, in turn, activates phosphodiesterase.
  7. Phosphodiesterase breaks down cGMP to 5'-GMP. This lowers the concentration of cGMP and therefore the sodium channels close.
  8. Closure of the sodium channels causes hyperpolarisation of the cell due to the ongoing potassium current.
  9. Hyperpolarisation of the photoreceptor results in a decrease in the amount of the neurotransmitter glutamate that is released by the cell.
  10. A decrease in the amount of glutamate released by the photoreceptors causes depolarization of On center bipolar cells (rod and cone On bipolar cells) and hyperpolarization of cone Off bipolar cells.

Back to the beginning

Transducin inactivates itself. It does this by hydrolysing the GTP that activated it with its own innate GTPase activity.

Rhodopsin becomes a target for phosphorylation by a specific protein kinase, opsin kinase. Arrestin then interacts with the phosphorylated rhodopsin and inactivates it.

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.

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