Rod cell

Neuron: Rod cell
Cross section of the retina. Rods are visible at far right.
Location	Retina
Function	Low light photoreceptor
Morphology	rod shaped
Presynaptic connections	None
Postsynaptic connections	Bipolar Cells and Horizontal cells
NeuroLex ID	sao1458938856
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Rod cells, or rods, are photoreceptor cells in the retina of the eye that can function in less intense light than can the other type of photoreceptor, cone cells. Named for their cylindrical shape, rods are concentrated at the outer edges of the retina and are used in peripheral vision. There are about 90 million rod cells in the human retina. More sensitive than cone cells, rod cells are almost entirely responsible for night vision.

Structure and function

Rods are a little narrower than cones but have the same structural basis. The pigment is on the outer side, lying on the pigment epithelium. This end contains many stacked disks, probably from the folding inward of the limiting membrane surrounding this section, allowing a higher area for visual pigment and increasing the efficiency of light absorption. Because they have only one type of light-sensitive pigment, rather than the three types that human cone cells have, rods have little, if any, role in color vision.

Like cones, rod cells have a synaptic terminal, an inner segment, and an outer segment. The synaptic terminal forms a synapse with another neuron, for example a bipolar cell. The inner and outer segments are connected by a cilium.^[1] The inner segment contains organelles and the cell's nucleus, while the rod outer segment (abbreviated to ROS), which is pointed toward the back of the eye, contains the light-absorbing materials.^[1]

Sensitivity

A rod cell is sensitive enough to respond to a single photon of light^{[citation needed]}, and is about 100 times more sensitive to a single photon than cones. Rods require less light to function than cones, they are therefore the primary source of visual information at night (scotopic vision). Cone cells, on the other hand, require tens to hundreds of photons to become activated. Additionally, multiple rod cells converge on a single interneuron, collecting and amplifying the signals. However, this convergence comes at a cost to visual acuity (or image resolution) because the pooled information from multiple cells is less distinct than it would be if the visual system received information from each rod cell individually. The convergence of rod cells also tends to make peripheral vision very sensitive to movement, and is responsible for the phenomenon of an individual seeing something vague occur out of the corner of his or her eye.

Rod cells also respond more slowly to light than cones do, so stimuli they receive are added over about 100 milliseconds. While this makes rods more sensitive to smaller amounts of light, it also means that their ability to sense temporal changes, such as quickly changing images, is less accurate than that of cones.^[1]

Experiments by George Wald and others showed that rods are most sensitive to wavelengths of light around 498 nm (green-blue), and are completely insensitive to wavelengths longer than about 640 nm (red). This fact is responsible for the Purkinje effect, in which blue colors appear more intense relative to reds at twilight, when rods take over as the cells responsible for vision.

Response to light

Anatomy of a Rod Cell^[2]

Activation of a single molecule of rhodopsin, the photosensitive pigment in rods, can lead to a large reaction in the cell because the signal is amplified. Once activated, rhodopsin can activate hundreds of transducin molecules, each of which in turn activate a phosphodiesterase molecule, which can break down over a thousand cGMP molecules per second.^[1] Thus rods can have a large response to a small amount of light.

As the retinal component of rhodopsin is derived from vitamin A, a deficiency of vitamin A causes a deficit in the pigment needed by rod cells. Consequently, fewer rod cells are able to sufficiently respond in darker conditions, and as the cone cells are poorly adapted for sight in the dark, blindness can result. This is night-blindness.

Revert to the resting state

Rods make use of three inhibitory mechanisms (negative feedback mechanisms) to allow a rapid revert to the resting state after a flash of light.

Firstly, there exists a rhodopsin kinase (RK) which would phosphorylate the cytosolic tail of the activated rhodopsin on the multiple serines, partially inhibiting the activation of transducin. Also, an inhibitory protein - arrestin then binds to the phosphorylated rhodopsins to further inhibit the rhodopsin's activity.

While arrestin shuts off rhodopsin, an RGS protein (functioning as a GTPase-activiating proteins(GAPs)) drives the transducin (G-protein) into an "off" state by increasing the rate of hydrolysis of the bounded GTP to GDP.

Also as the cGMP sensitive channels allow not only the influx of sodium ions, but also calcium ions, with the decrease in concentration of cGMP, cGMP sensitive channels are then closed and reducing the normal influx of calcium ions. The decrease in the concentration of calcium ions stimulates the calcium ion-sensitive proteins, which would then activiate the guanylyl cyclase to replenish the cGMP, rapidly restoring its original concentration. The restoration opens the cGMP sensitive channels and causes a depolarization of the plasma membrane.^[3]

Desensitization

When the rods are exposed to a high concentration of photons for a prolonged period, they become desensitized (adapted) to the environment.

As rhodopsin is phosphorylated by rhodopsin kinase (a member of the GPCR kinases(GRKs)), it binds with high affinity to the arrestin. The bound arrestin can contribute to the desensitization process in at least two ways. First, it prevents the interaction between the G protein and the activated receptor. Second, it serves as an adaptor protein to aid the receptor to the clathrin-dependent endocytosis machinery (to induce receptor-mediated endocytosis).^[3]

References

1. ^ ^{a b c d} Kandel E.R., Schwartz, J.H., Jessell, T.M. (2000). Principles of Neural Science, 4th ed., pp.507-513. McGraw-Hill, New York.
2. ^ Human Physiology and Mechanisms of Disease by Arthur C. Guyton (1992) p.373
3. ^ ^{a b} Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, Peter Walter (2008). Molecular Biology of The Cell, 5th ed., pp.919-921. Garland Science.

External links

• NIF Search - Rod Cell via the Neuroscience Information Framework

See also

• Sensory receptor