Why rods and cones

Researchers are investigating this ion channel as a potential explanation behind cone-rod dystrophy, an inherited disease that can cause vision loss over time. Michael W. Richardson Michael W. Richardson is a writer and editor based in Brooklyn, New York, covering topics ranging from the brain and behavior to the environment.

See how discoveries in the lab have improved human health. Read More. For Educators Log in. The human eye has over million rod cells. Cones require a lot more light and they are used to see color.

We have three types of cones: blue, green, and red. The human eye only has about 6 million cones. Many of these are packed into the fovea, a small pit in the back of the eye that helps with the sharpness or detail of images.

Other animals have different numbers of each cell type. Animals that have to see in the dark have many more rods than humans have. Take a close look at the photoreceptors in the drawings above and below. The disks in the outer segments to the right are where photoreceptor proteins are held and light is absorbed. Rods have a protein called rhodopsin and cones have photopsins. But wait That means that the light is absorbed closer to the outside of the eye. Aren't these set up backwards?

What is going on here? Light moves through the eye and is absorbed by rods and cones at the back of the eye. Click for more information. First of all, the discs containing rhodopsin or photopsin are constantly recycled to keep your visual system healthy.

By having the discs right next to the epithelial cells retinal pigmented epithelium: RPE at the back of the eye, parts of the old discs can be carried away by cells in the RPE.

Another benefit to this layout is that the RPE can absorb scattered light. This means that your vision is a lot clearer. Light can also have damaging effects, so this set up also helps protect your rods and cones from unnecessary damage.

While there are many other reasons having the discs close to the RPE is helpful, we will only mention one more. Think about someone who is running a marathon.

In order to keep muscles in the body working, the runner needs to eat special nutrients or molecules during the race. Rods and cones are similar, but instead of running, they are constantly sending signals. The reason stems from a single property that the ancestral rods developed: the ability to respond reliably to individual photons of light.

In cones, the on-going cellular noise is large, and completely swamps the response to a single photon. However, in rods, the amplitude of the single-photon response substantially exceeds the cellular noise level and is reliably detectable above that noise. How has this been beneficial to the organism? By permitting the evolution of retinal circuitry that can process these single-photon events, thereby providing scotopic visual sensitivity orders of magnitude better than in the cone system.

As a result, a dark-adapted human subject can detect just a handful of photons hitting the retina. The synapse from the rod photoreceptor is reliably able to transmit the discrete quantal responses to the rod bipolar cell RBC , as discovered from measurements of ERG b -wave sensitivity 12 and from single-cell recordings.

Remarkably, this cascade is broadly similar to that used in phototransduction and, as in the case of rhabdomeric photoreceptors, the final stage involves a TRP ion channel.

This rod synapse appears to operate in a thresholding mode, substantially removing the ongoing photoreceptor dark noise. It is instructive to consider what happens in total darkness. Thus, the RBCs send their output to a dedicated class of amacrine cells, the AII amacrines, that inject their signals into the cone pathway shown on the right in Figure 1 at the level of the cone bipolar cells and their synapses onto retinal ganglion cells. The beauty of this arrangement is that it provides a common output pathway for rod and cone signals, yet it avoids introducing synaptic noise into the cone circuitry when the rods are saturated.

Simplified schematic of cone and rod pathways through the retina. Right-hand side shows the cone pathway and left-hand side shows the main scotopic rod pathway that provides input to the cone pathway. The AII amacrine provides sign-conserving input via connexin gap junctions onto ON cone bipolar cell terminals, as well as sign-inverting glycinergic input onto OFF cone bipolar cell terminals, thereby providing push—pull signals to ON and OFF ganglion cells.

The sign-inverting glutamate synapses from cones to cone ON bipolar cells, and from rods to rod bipolar cells use a metabotropic postsynaptic mechanism involving a G-protein cascade, whereas the other chemical synapses use ionotropic mechanisms.

Light hyperpolarises the photoreceptors, so that the sign-inverting synapse generates a depolarising light response in the ON cone bipolar cell and rod bipolar cell. Not shown in this diagram are surround mechanisms and lateral interactions mediated by horizontal cells and other classes of amacrine cell, or rod pathways used at mesopic levels modified from Robson and Frishman; 12 see Demb and Singer 19 for recent review.

Electrophysiological recordings made many decades ago showed that under fully dark-adapted conditions, a cat retinal ganglion cell is able to fire additional spikes when just a few photoisomerisations occur within its receptive field.

The performance of rods and scotopic vision is inferior to that of cones and photopic vision in a variety of ways, as indicated in Table 1.

Some of these deficiencies represent consequences of the need for the retina to be able to process individual photon responses at the very lowest intensities. Likewise, the very slow dark adaptation of scotopic visual sensitivity following large bleaches has an explanation that involves the exceedingly low final dark-adapted threshold that is achieved by processing single-photon signals. The time course of human dark adaptation is plotted in Figure 2 for recovery after exposures that bleached from 0.

Psychophysical dark adaptation recovery for a normal human subject. The symbols plot measurements of log threshold elevation, following intense exposures that bleached from 0. Horizontal dashed line indicates the cone plateau at 3.

Grey curves plot the predicted decline of log threshold elevation for a model in which opsin recombines with cis retinal produced by a rate-limited enzymatic reaction representing, eg, RDH5 or RPE65 activity. Characteristically, the time course of decline of scotopic log threshold follows straight-line kinetics, indicated by the parallel grey curves, over a mid-range of thresholds across all bleaching levels.

Why does recovery take so long? The first crucial point to note is that, in this regime, the threshold elevation is not remotely caused by the lack of rhodopsin available to absorb photons.

Instead, the elevation of threshold is caused by the presence of a product of rhodopsin bleaching. As time progresses after a bleach, cis retinal recombines with opsin, so that the quantity of free opsin steadily declines, thereby causing a corresponding decline in equivalent background intensity and scotopic threshold. Why does the elimination of opsin not occur more rapidly than this? In order to achieve speedier regeneration of rhodopsin, the delivery of cis retinaldehyde would need to be faster, and this would generate a higher concentration of the retinoid.

However, this aldehyde is potentially toxic, and a high concentration over the long term would be likely to cause retinal damage. On the other hand, the actual speed of dark adaptation is probably just sufficient to have prevented a survival disadvantage over evolutionary times. Indeed, it appears that the time course of human dark adaptation is matched to the fading of light at dusk on this planet, suggesting that the delivery of cis retinaldehyde has been adjusted to a level sufficient to accomplish this, without creating a concentration so high as to cause toxicity.

The speed of scotopic dark adaptation is potentially an important predictor of the approaching onset of AMD. Finally, why does attainment of full dark adaptation takes so much longer for the rod system than for the cone system?

Two factors seem relevant. However, secondly, the dark-adapted scotopic threshold is more than 3 orders of magnitude lower than the photopic threshold cone plateau. How did the ability to process single-photon signals arise? To examine this, we need to consider the evolution of the vertebrate eye, and indeed the evolution of vertebrates, as summarised schematically in Figure 3.

Evolution of vertebrates and the vertebrate camera-style eye. The origin of vertebrates is shown, over a timescale from roughly to millions of years ago Mya. The red curve indicates our direct ancestors, beginning with early metazoans; dashed curves indicate extinct taxa of potential interest.

Our last common ancestor with tunicates is presumed to have had no more than a simple eye-spot ocellus , whereas our last common ancestor with lampreys is presumed to have had a camera-style eye.

The anatomy and physiology of retinal photoreceptors, and of the retinal circuitry and camera-style eye, bear extremely close homology across all jawed vertebrates. Furthermore, this remarkable homology extends even to the jawless lampreys. The homologies are so extensive that they lead to the inescapable conclusion that the last common ancestor that we share with lampreys already possessed fundamentally the same camera-style eye that we possess, with homologous though not identical photoreceptors.

We will return to this later on when we discuss color vision and color blindness. The Receptor Mosaic. This figure shows how the three cone types are arranged in the fovea. Currently there is a great deal of research involving the determination of the ratios of cone types and their arrangement in the retina. This diagram was produced based on histological sections from a human eye to determine the density of the cones.

The L-cone:M-cone ratio was set to 1. This is a reasonable number considering that recent studies have shown wide ranges of cone ratios in people with normal color vision. In the central fovea an area of approximately 0. The S-cones are semi-regularly distributed and the M- and L-cones are randomly distributed. Throughout the whole retina the ratio of L- and M- cones to S-cones is about Spatial Acuity Estimate From Mosaic.

From the cone mosaic we can estimate spatial acuity or the ability to see fine detail. The distance between cone centers in the hexagonal packing of the cones is about 0. To convert this to degrees of visual angle you need to know that there are 0. The Nyquist frequency, f , is the frequency at which aliasing begins. In actuality, the foveal Nyquist limit is more like 60 cycles per degree. This may be a result of the hexagonal rather than the rectangular packing of the cone mosaic.

The optics of the eye blur the retinal image so that this aliasing is not produced.