What do rods and cones do

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.

The lamprey retina has a three-layered structure closely resembling that in gnathostomes, 31 and lamprey photoreceptors utilise the same five classes of visual opsin as used by gnathostomes. However, there have not yet been reports to indicate whether the lamprey retina has the ability to operate in a photon-processing mode. On the other hand, it has long been known that the response properties of dogfish retinal bipolar cells are closely comparable to those of mammalian RBCs, 35 and that deep-sea fish exhibit extremely high visual sensitivity.

The retina was three layered and processed signals in broadly the same way as is done in the photopic division of the modern vertebrate retina, providing dichromatic colour vision in daylight lighting levels. A descendant of this creature underwent genome quadruplication through two rounds of WGD, and it was this quadruplication of genes that provided the flexibility that enabled the massive radiation of vertebrate species.

In the retina, this quadruplication led to the advent of four classes of cone opsin 3 SWS and 1 LWS , with individual spectra covering the whole of the visible region.

In addition, the photoreceptor expressing the fourth of the quadruplicated SWS opsins Rh1 became specialised for operation at very low intensities night-time and in the deep ocean , and eventually achieved the ability to reliably detect individual photons of light: this cell became the ancestral rod photoreceptor.

Presented with these quantal signals from rods, the retina at some stage evolved the ability to process them as discrete signals, rather than as analogue signals, and thereby achieved a huge advantage in extending the visual threshold down to exceedingly low levels. The circuitry that evolved to accomplish this discrete signalling utilised rod bipolar cells and AII amacrine cells that were piggy-backed onto the pre-existing photopic retinal signalling pathway.

Topography of the layer of rods and cones in the human retina. Acta Ophthalmol ; 13 S6 : 1— Google Scholar. Human photoreceptor topography. Read More. For Educators Log in. Image of the Week. About the Author. Yaeger, Roupen A. Khanjian and Teresa Puthussery. Journal of Neuroscience. The rod is more sensitive than the cone. This is why you are still able to perceive shapes and some objects even in dim light or no light at all.

In addition to being the receptor that allows you to see in the dark, the rod is also the better motion sensor since it is more sensitive in nature, and has more individual receptors than the cone. This figure shows the sequence of the L- and M-cone pigments compared to each other.

These pigments are very similar. Only those differences within the cell membrane can contribute to the differences in their spectral sensitivity. The M- and L- cone pigments are both encoded on the X chromosome in tandem. The 23rd pair of chromosomes determines gender.

For females this pair is XX and for males this pair is XY. 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.