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Photoreceptor cell

From Wikipedia, the free encyclopedia

Photoreceptor cell
1414 Rods and Cones.jpg
Functional parts of the rods and cones, which are two of the three types of photosensitive cells in the retina
NeuroLex IDsao226523927
Anatomical terms of neuroanatomy

A photoreceptor cell is a specialized type of neuroepithelial cell found in the retina that is capable of visual phototransduction. The great biological importance of photoreceptors is that they convert light (visible electromagnetic radiation) into signals that can stimulate biological processes. To be more specific, photoreceptor proteins in the cell absorb photons, triggering a change in the cell's membrane potential.

There are currently three known types of photoreceptor cells in mammalian eyes: rods, cones, and photosensitive retinal ganglion cells. The two classic photoreceptor cells are rods and cones, each contributing information used by the visual system to form a representation of the visual world, sight. The rods are narrower than the cones and distributed differently across the retina, but the chemical process in each that supports phototransduction is similar.[1] A third class of mammalian photoreceptor cell was discovered during the 1990s:[2] the photosensitive ganglion cells. These cells do not contribute to sight directly, but are thought to support circadian rhythms and pupillary reflex.

There are major functional differences between the rods and cones. Rods are extremely sensitive, and can be triggered by a single photon.[3][4] At very low light levels, visual experience is based solely on the rod signal. This explains why colors cannot be seen at low light levels: only one type of photoreceptor cell is active.

Cones require significantly brighter light (i.e., a larger number of photons) in order to produce a signal. In humans, there are three different types of cone cell, distinguished by their pattern of response to different wavelengths of light. Color experience is calculated from these three distinct signals, perhaps via an opponent process.[5] The three types of cone cell respond (roughly) to light of short, medium, and long wavelengths. Note that, due to the principle of univariance, the firing of the cell depends upon only the number of photons absorbed. The different responses of the three types of cone cells are determined by the likelihoods that their respective photoreceptor proteins will absorb photons of different wavelengths. So, for example, an L cone cell contains a photoreceptor protein that more readily absorbs long wavelengths of light (i.e., more "red"). Light of a shorter wavelength can also produce the same response, but it must be much brighter to do so.

The human retina contains about 120 million rod cells, and 6 million cone cells. The number and ratio of rods to cones varies among species, dependent on whether an animal is primarily diurnal or nocturnal. Certain owls, such as the nocturnal tawny owl,[6] have a tremendous number of rods in their retinae. In the human visual system, in addition to the photosensitive rods & cones, there are about 2.4 million to 3 million ganglion cells, with 1 to 2% of them being photosensitive. The axons of ganglion cells form the two optic nerves.

Photoreceptor cells are typically arranged in an irregular but approximately hexagonal grid, known as the retinal mosaic.

The pineal and parapineal glands are photoreceptive in non-mammalian vertebrates, but not in mammals. Birds have photoactive cerebrospinal fluid (CSF)-contacting neurons within the paraventricular organ that respond to light in the absence of input from the eyes or neurotransmitters.[7] Invertebrate photoreceptors in organisms such as insects and molluscs are different in both their morphological organization and their underlying biochemical pathways. Described here are human photoreceptors.

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Take a good long look at this -- we’re gonna mess with your brain. This is the first stage of an optical illusion. Many illusions use patterns of light or perspective to exploit the disconnect that exists between sensation and perception -- between what your eyes see and what your brain understands. But not all illusions work that way. Some produce ghost effects, or afterimages, that take advantage of glitches in the physiology of human vision. Like this flag. I’m not trying to make a political statement here. And I’m not going ask you to swear allegiance to the Republic of Hank or anything. I mean, if I was gonna start my own country, my flag would be way cooler than that -- not that I’ve thought about that a lot. And now, look at this white screen. If you looked at that flag for at least 30 seconds without moving your eyes, you’ll see something, even though this screen is blank -- an afterimage of the flag. But instead of being turquoise, and black, and yellow, it’s red, white, and blue. OK so that’s pretty cool, but I’m not here just to entertain you. This kind of illusion is actually a great way to explain your very complex sense of vision. And I do mean complex… nearly 70 percent of all the sensory receptors in your whole body are in the eyes! Not only that, but in order for you to see, perceive, and recognize something -- whether it’s a flag or a handsome guy in glasses and a sport coat sitting behind a desk -- nearly half of your entire cerebral cortex has to get involved. Vision is considered the dominant sense of humans and while we can get along without it and it can be tricked, what you are about to learn is NOT an illusion. When we talked about your sense of hearing, we began with the mechanics of sound. So before we get to how your eyeballs work, it makes sense to talk about what they’re actually seeing -- light bouncing off of stuff. Light is electromagnetic radiation traveling in waves. Remember how the pitch and loudness of a sound is determined by the frequency and amplitude of its wave? Well, it’s kind of similar with light, except that the frequency of a light wave determines its hue, while the amplitude relates to its brightness. We register short waves at high frequencies as bluish colors, while long, low frequencies look reddish to us. Meanwhile, that red might appear dull and muted if the wave is moving at a lower amplitude, but super bright if the wave has greater amplitude and thus higher intensity. But the visible light we’re able to see is only a tiny chunk of the full electromagnetic spectrum, which ranges from short gamma and X rays all the way to long radio waves. Just as the ear’s mechanoreceptors or the tongue’s chemoreceptors convert sounds and chemicals into action potentials, so too do your eyes’ photoreceptors convert light energy into nerve impulses that the brain can understand. To figure out how all this works, let’s start with understanding some eye anatomy. Some of the first things you’ll notice around your average pair of eyes are all the outer accessories -- like the eyebrows that help keep the sweat away if you forgot your headband at raquetball, and the super-sensitive eyelashes that trigger reflexive blinking, like if you’re on a sandy beach in a windstorm. These features, along with the eyelids and tear-producing lacrimal apparatus are there to help protect your fragile eyeballs. The eyeball itself is irregularly spherical, with an adult diameter of about 2.5 centimeters. It’s essentially hollow -- full of fluids that help it keep its shape -- and you can really only see about the anterior sixth of the whole ball. The rest of it is tucked into a pocket of protective fat, tethered down by six straplike extrinsic eye muscles, and jammed into the bony orbit of your skull. While all this gear generally does a fantastic job of keeping your eyeballs inside of your head (which is good), on very rare occasions, perhaps after head trauma or -- or even a really intense sneeze! -- those suckers can pop right out -- a condition called globe luxation, which you really do not want to google. I’ll just sit here while you Google it. Now, you don’t need to pop out an eyeball in order to learn how it’s structured. I’ll save you the trouble and tell you that its wall is made up of three distinct layers -- the fibrous, vascular, and inner layers. The outermost fibrous layer is made of connective tissue. Most of it is that white stuff called the sclera, while the most anterior part is the transparent cornea. The cornea is like the window that lets light into the eye, and if you’ve ever experienced the excruciating pain of a scratched one, you know how terrible it can be to damage something so loaded with pain receptors. Going down a little deeper, the wall’s middle vascular layer contains the posterior choroid, a membrane that supplies all of the layers with blood. In the anterior, there’s also the ciliary body, a ring of muscle tissue that surrounds the lens; but the most famous part of this middle layer is the iris. The iris is that distinctive colored part of the eye that is uniquely yours. It’s made up of smooth muscle tissue, shaped liked a flattened donut, and sandwiched between the cornea and the lens. Those circular sphincter muscles -- yeah, that’s right, you’ve got sphincters everywhere! -- contract and expand, changing the size of the dark dot of your pupil. The pupil itself is just the opening in the iris that allows light to travel into the eye. You can see how an iris protects the eye from taking too much light in if you shine a flashlight in your friend’s eye in a dark room. Their pupils will go from dilated to pinpoints in a couple of seconds. Light comes in through the cornea and pupil and hits the lens -- the convex, transparent disc that focuses that light and projects it onto the retina, which makes up the inner layer of the back of the eyeball. Your retinas are loaded with millions of photoreceptors which do the crucial work of converting light energy into the electrical signals that your brain will receive. These receptor cells come in two flavors -- rods and cones -- which I’ll come back to in a minute. But the retina itself has two layers, the outer pigmented layer that helps absorb light so it doesn't scatter around the eyeball, and the inner neural layer. And this layer, as the name indicates, contains neurons -- not only the photoreceptors but also bipolar neurons and ganglion neurons. These two kinds of nerve cells combine to produce a sort of pathway for light, or at least data about light. Bipolar neurons have synapses at both ends, forming a kind of bridge -- on one end it synapses with a photoreceptor, and at the other, it synapses with a ganglionic neuron, which goes on to form the optic nerve. So, say you’ve just been hit with a blinding flashlight beam. That light hits your posterior retina and spreads from the photoreceptors to the bipolar cells just beneath them, to the innermost ganglion cells, where they then generate action potentials. The axons of all those ganglion cells weave together to create the thick, ropey optic nerve -- your second cranial nerve -- which leaves the back of your eyeball and carries those impulses up to the thalamus and then on to the brain’s visual cortex. So that’s the basic anatomy and event sequencing of human vision, but what I really want to talk about are those two types of photoreceptors -- your rods and your cones. Cones sit near the retina’s center, and detect fine detail and color. They can be divided into red, green, and blue-sensitive types, based on how they respond to different types of light. But they’re not very sensitive, and they really only hit their activation thresholds in bright conditions. Rods, on the other hand, are more numerous more light-sensitive. But they can’t pick up real color. Instead they only register a grayscale of black and white. They hang out around the edges of your retinas, and rule your peripheral vision. Since these receptors function so differently, you might not be surprised to learn that your rods and cones are also wired to your retinas in different ways. As many as 100 different rods may connect to a single ganglion cell -- but because they all send their information to the ganglion at once, the brain can’t tell which individual rods have been activated. That’s why they’re not very good at providing detailed images -- all they can really do is give you information about objects general shape, or whether it’s light or dark. Each cone, by contrast, gets its own personal ganglion cell to hook up with, which allows for very detailed color vision, at least if conditions are bright enough. And all this brings us back to that weird flag. Why does staring at this flag and then looking at an empty white space make us see a phantom flag of different colors? Well, it begins with the fact that our photoreceptors can make us see afterimages. Some stimuli, like really brilliant colors or really bright lights, are so strong that our photoreceptors will continue firing action potentials even after we close our eyes or look away. The other part of the illusion has to do with another bug in our visual programming: And it’s just that our cones can just get tired. If you stare long enough at a brightly colored image, your cones will receive the same stimulus for too long, and basically stop responding. In the case of the flag, you looked at an image with bright turquoise stripes. Because your retinas contain red, green, and blue-sensitive cones, the blue and green ones got tired after a while, leaving only the red cones left to fire. Then, you looked at the white screen. That white light included all of colors and wavelengths of visible light. So, your eyes were still receiving red, green, and blue light -- but only the red cones were able to respond. As a result, when the afterimage began to appear, those stripes looked red. The same thing happened to your rods. Except, since they only register black and white, the afterimage was like looking at a negative of a photograph -- dark replaced with light. That’s how those black stars and stripes turned white. So, yes, human vision is fallible, but those mistakes that it makes can help us understand that wonderfully complex system. And that wonderfully complex system probably helped you learn about the anatomy and physiology of vision today, starting with the structure of the eye and its three layers: the fibrous, vascular, and inner layers. We spent most of our time exploring the inner layer, which consists of the retina and its three kinds of neurons: photoreceptors, bipolar cells, and ganglion neurons. And after learning how to tell our rods from our cones, we then dissected how the weird flag illusion works. Special thanks to our Headmaster of Learning, Thomas Frank for his support of Crash Course and free education. And thank you to all of our Patreon patrons who make Crash Course possible through their monthly contributions. If you like Crash Course and want to help us keep making great new videos, you can check out to see all of the cool things that we’ve made available to you. Crash Course is filmed in the Doctor Cheryl C. Kinney Crash Course Studio. This episode was written by Kathleen Yale, edited by Blake de Pastino, and our consultant, is Dr. Brandon Jackson. Our director is Nicholas Jenkins, the script supervisor and editor is Nicole Sweeney, Michael Aranda is our sound designer, and the graphics team is Thought Café



Anatomy of cones and rods varies slightly.

Rod and cone photoreceptors are found on the outermost layer of the retina; they both have the same basic structure. Closest to the visual field (and farthest from the brain) is the axon terminal, which releases a neurotransmitter called glutamate to bipolar cells. Farther back is the cell body, which contains the cell's organelles. Farther back still is the inner segment, a specialized part of the cell full of mitochondria. The chief function of the inner segment is to provide ATP (energy) for the sodium-potassium pump. Finally, closest to the brain (and farthest from the field of view) is the outer segment, the part of the photoreceptor that absorbs light. Outer segments are actually modified cilia[9][10] that contain disks filled with opsin, the molecule that absorbs photons, as well as voltage-gated sodium channels.

The membranous photoreceptor protein opsin contains a pigment molecule called retinal. In rod cells, these together are called rhodopsin. In cone cells, there are different types of opsins that combine with retinal to form pigments called photopsins. Three different classes of photopsins in the cones react to different ranges of light frequency, a differentiation that allows the visual system to calculate color. The function of the photoreceptor cell is to convert the light energy of the photon into a form of energy communicable to the nervous system and readily usable to the organism: This conversion is called signal transduction.

The opsin found in the photosensitive ganglion cells of the retina is called melanopsin. These cells are involved in various reflexive responses of the brain and body to the presence of (day)light, such as the regulation of circadian rhythms, pupillary reflex and other non-visual responses to light. Melanopsin functionally resembles invertebrate opsins.

When light activates the melanopsin signaling system, the melanopsin-containing ganglion cells discharge nerve impulses that are conducted through their axons to specific brain targets. These targets include the olivary pretectal nucleus (a center responsible for controlling the pupil of the eye), the LGN, and, through the retinohypothalamic tract (RHT), the suprachiasmatic nucleus of the hypothalamus (the master pacemaker of circadian rhythms). Melanopsin-containing ganglion cells are thought to influence these targets by releasing from their axon terminals the neurotransmitters glutamate and pituitary adenylate cyclase activating polypeptide (PACAP).


Normalized human photoreceptor absorbances for different wavelengths of light[11]
Normalized human photoreceptor absorbances for different wavelengths of light[11]
Illustration of the distribution of cone cells in the fovea of an individual with normal color vision (left), and a color blind (protanopic) retina. Note that the center of the fovea holds very few blue-sensitive cones.
Illustration of the distribution of cone cells in the fovea of an individual with normal color vision (left), and a color blind (protanopic) retina. Note that the center of the fovea holds very few blue-sensitive cones.
Distribution of rods and cones along a line passing through the fovea and the blind spot of a human eye[12]
Distribution of rods and cones along a line passing through the fovea and the blind spot of a human eye[12]

The human retina has approximately 6 million cones and 120 million rods.[13] Signals from the rods and cones converge on ganglion and bipolar cells for preprocessing before they are sent to the lateral geniculate nucleus. At the "center" of the retina (the point directly behind the lens) lies the fovea (or fovea centralis), which contains only cone cells; and is the region capable of producing the highest visual acuity or highest resolution. Across the rest of the retina, rods and cones are intermingled. No photoreceptors are found at the blind spot, the area where ganglion cell fibers are collected into the optic nerve and leave the eye.[14]

The photoreceptor proteins in the three types of cones differ in their sensitivity to photons of different wavelengths (see graph). Since cones respond to both the wavelength and intensity of light, the cone's sensitivity to wavelength is measured in terms of its relative rate of response if the intensity of a stimulus is held fixed, while the wavelength is varied. From this, in turn, is inferred the absorbance.[15] The graph normalizes the degree of absorbance on a hundred-point scale. For example, the S cone's relative response peaks around 420 nm (nanometers, a measure of wavelength). This tells us that an S cone is more likely to absorb a photon at 420 nm than at any other wavelength. If light of a different wavelength to which it is less sensitive, say 480 nm, is increased in brightness appropriately, however, it will produce exactly the same response in the S cone. So, the colors of the curves are misleading. Cones cannot detect color by themselves; rather, color vision requires comparison of the signal across different cone types.


The process of phototransduction occurs in the retina.[13] The retina has many layers of various cell types.[13] The best-known photoreceptor cells (rods and cones) form the outermost layer. They are the photoreceptors responsible for sight. The middle layer contains bipolar cells, which collect neural signals from the rods and the cones and then transmit them to the innermost layer of the retina,[13] where the neurons called retinal ganglion cells (RGCs), a small percentage of which are themselves photosensitive, organize the signals and send them to the brain.[13]

Activation of rods and cones is actually hyperpolarization; when they are not being stimulated, they depolarize and release glutamate continuously. In the dark, cells have a relatively high concentration of cyclic guanosine 3'-5' monophosphate (cGMP), which opens ion channels (largely sodium channels, though calcium can enter through these channels as well). The positive charges of the ions that enter the cell down its electrochemical gradient change the cell's membrane potential, cause depolarization, and lead to the release of the neurotransmitter glutamate. Glutamate can depolarize some neurons and hyperpolarize others.

When light hits a photoreceptive pigment within the photoreceptor cell, the pigment changes shape. The pigment, called iodopsin or rhodopsin, consists of large proteins called opsin (situated in the plasma membrane), attached to a covalently bound prosthetic group: an organic molecule called retinal (a derivative of vitamin A). The retinal exists in the 11-cis-retinal form when in the dark, and stimulation by light causes its structure to change to all-trans-retinal. This structural change causes it to activate a regulatory protein called transducin, which leads to the activation of cGMP phosphodiesterase, which breaks cGMP down into 5'-GMP. Reduction in cGMP allows the ion channels to close, preventing the influx of positive ions, hyperpolarizing the cell, and stopping the release of neurotransmitters.[16] The entire process by which light initiates a sensory response is called visual phototransduction.

Dark current

Unstimulated (in the dark), cyclic-nucleotide gated channels in the outer segment are open because cyclic GMP (cGMP) is bound to them. Hence, positively charged ions (namely sodium ions) enter the photoreceptor, depolarizing it to about −40 mV (resting potential in other nerve cells is usually −65 mV). This depolarizing current is often known as dark current.

Signal transduction pathway

The absorption of light leads to an isomeric change in the retinal molecule.
The absorption of light leads to an isomeric change in the retinal molecule.

The signal transduction pathway is the mechanism by which the energy of a photon signals a mechanism in the cell that leads to its electrical polarization. This polarization ultimately leads to either the transmittance or inhibition of a neural signal that will be fed to the brain via the optic nerve. The steps, or signal transduction pathway, in the vertebrate eye's rod and cone photoreceptors are then:

  1. The rhodopsin or iodopsin in the disc membrane of the outer segment absorbs a photon, changing the configuration of a retinal Schiff base cofactor inside the protein from the cis-form to the trans-form, causing the retinal to change shape.
  2. This results in a series of unstable intermediates, the last of which binds stronger to a G protein in the membrane, called transducin, and activates it. This is the first amplification step – each photoactivated rhodopsin triggers activation of about 100 transducins.
  3. Each transducin then activates the enzyme cGMP-specific phosphodiesterase (PDE).
  4. PDE then catalyzes the hydrolysis of cGMP to 5' GMP. This is the second amplification step, where a single PDE hydrolyses about 1000 cGMP molecules.
  5. The net concentration of intracellular cGMP is reduced (due to its conversion to 5' GMP via PDE), resulting in the closure of cyclic nucleotide-gated Na+ ion channels located in the photoreceptor outer segment membrane.
  6. As a result, sodium ions can no longer enter the cell, and the photoreceptor outer segment membrane becomes hyperpolarized, due to the charge inside the membrane becoming more negative.
  7. This change in the cell's membrane potential causes voltage-gated calcium channels to close. This leads to a decrease in the influx of calcium ions into the cell and thus the intracellular calcium ion concentration falls.
  8. A decrease in the intracellular calcium concentration means that less glutamate is released via calcium-induced exocytosis to the bipolar cell (see below). (The decreased calcium level slows the release of the neurotransmitter glutamate, which excites the postsynaptic bipolar cells and horizontal cells.)
  9. Reduction in the release of glutamate means one population of bipolar cells will be depolarized and a separate population of bipolar cells will be hyperpolarized, depending on the nature of receptors (ionotropic or metabotropic) in the postsynaptic terminal (see receptive field).

Thus, a rod or cone photoreceptor actually releases less neurotransmitter when stimulated by light. Less neurotransmitter in the synaptic cleft between a photoreceptor and bipolar cell will serve to either excite (depolarize) ON bipolar cells or inhibit (hyperpolarize) OFF bipolar cells. Thus, it is at the photoreceptor-bipolar cell synapse where visual signals are split into ON and OFF pathways.[17]

ATP provided by the inner segment powers the sodium-potassium pump. This pump is necessary to reset the initial state of the outer segment by taking the sodium ions that are entering the cell and pumping them back out.

Although photoreceptors are neurons, they do not conduct action potentials with the exception of the photosensitive ganglion cell – which are involved mainly in the regulation of circadian rhythms, melatonin, and pupil dilation.


Phototransduction in rods and cones is somewhat unusual in that the stimulus (in this case, light) reduces the cell's response or firing rate, different from most other sensory systems in which a stimulus increases the cell's response or firing rate. This difference has important functional consequences:

First, the classic (rod or cone) photoreceptor is depolarized in the dark, which means many sodium ions are flowing into the cell. Thus, the random opening or closing of sodium channels will not affect the membrane potential of the cell; only the closing of a large number of channels, through absorption of a photon, will affect it and signal that light is in the visual field. This system may have less noise relative to sensory transduction schema that increase rate of neural firing in response to stimulus, like touch and olfaction.

Second, there is a lot of amplification in two stages of classic phototransduction: one pigment will activate many molecules of transducin, and one PDE will cleave many cGMPs. This amplification means that even the absorption of one photon will affect membrane potential and signal to the brain that light is in the visual field. This is the main feature that differentiates rod photoreceptors from cone photoreceptors. Rods are extremely sensitive and have the capacity of registering a single photon of light, unlike cones. On the other hand, cones are known to have very fast kinetics in terms of rate of amplification of phototransduction, unlike rods.

Difference between rods and cones

Comparison of human rod and cone cells, from Eric Kandel et al. in Principles of Neural Science.[16]

Rods Cones
Used for scotopic vision (vision under low light conditions) Used for photopic vision (vision under high light conditions)
Very light sensitive; sensitive to scattered light Not very light sensitive; sensitive to only direct light
Loss causes night blindness Loss causes legal blindness
Low visual acuity High visual acuity; better spatial resolution
Not present in fovea Concentrated in fovea
Slow response to light, stimuli added over time Fast response to light, can perceive more rapid changes in stimuli
Have more pigment than cones, so can detect lower light levels Have less pigment than rods, require more light to detect images
Stacks of membrane-enclosed disks are unattached to cell membrane directly Disks are attached to outer membrane
About 120 million rods distributed around the retina[13] About 6 million cones distributed in each retina[13]
One type of photosensitive pigment Three types of photosensitive pigment in humans
Confer achromatic vision Confer color vision


Photoreceptors do not signal color; they only signal the presence of light in the visual field.

A given photoreceptor responds to both the wavelength and intensity of a light source. For example, red light at a certain intensity can produce the same exact response in a photoreceptor as green light of a different intensity. Therefore, the response of a single photoreceptor is ambiguous when it comes to color.

To determine color, the visual system compares responses across a population of photoreceptors (specifically, the three different cones with differing absorption spectra). To determine intensity, the visual system computes how many photoreceptors are responding. This is the mechanism that allows trichromatic color vision in humans and some other animals.


The key events mediating rod versus S cone versus M cone differentiation are induced by several transcription factors, including RORbeta, OTX2, NRL, CRX, NR2E3 and TRbeta2. The S cone fate represents the default photoreceptor program, however differential transcriptional activity can bring about rod or M cone generation. L cones are present in primates, however there is not much known for their developmental program due to use of rodents in research. There are five steps to developing photoreceptors: proliferation of multi-potent retinal progenitor cells (RPCs); restriction of competence of RPCs; cell fate specification; photoreceptor gene expression; and lastly axonal growth, synapse formation and outer segment growth.

Early Notch signaling maintains progenitor cycling. Photoreceptor precursors come about through inhibition of Notch signaling and increased activity of various factors including achaete-scute homologue 1. OTX2 activity commits cells to the photoreceptor fate. CRX further defines the photoreceptor specific panel of genes being expressed. NRL expression leads to the rod fate. NR2E3 further restricts cells to the rod fate by repressing cone genes. RORbeta is needed for both rod and cone development. TRbeta2 mediates the M cone fate. If any of the previously mentioned factors' functions are ablated, the default photoreceptor is a S cone. These events take place at different time periods for different species and include a complex pattern of activities that bring about a spectrum of phenotypes. If these regulatory networks are disrupted, retinitis pigmentosa, macular degeneration or other visual deficits may result.[18]


3D medical illustration of the rod and cone structure of photoreceptors.
3D medical illustration of the rod and cone structure of photoreceptors.

The rod and cone photoreceptors signal their absorption of photons via a decrease in the release of the neurotransmitter glutamate to bipolar cells at its axon terminal. Since the photoreceptor is depolarized in the dark, a high amount of glutamate is being released to bipolar cells in the dark. Absorption of a photon will hyperpolarize the photoreceptor and therefore result in the release of less glutamate at the presynaptic terminal to the bipolar cell.

Every rod or cone photoreceptor releases the same neurotransmitter, glutamate. However, the effect of glutamate differs in the bipolar cells, depending upon the type of receptor imbedded in that cell's membrane. When glutamate binds to an ionotropic receptor, the bipolar cell will depolarize (and therefore will hyperpolarize with light as less glutamate is released). On the other hand, binding of glutamate to a metabotropic receptor results in a hyperpolarization, so this bipolar cell will depolarize to light as less glutamate is released.

In essence, this property allows for one population of bipolar cells that gets excited by light and another population that gets inhibited by it, even though all photoreceptors show the same response to light. This complexity becomes both important and necessary for detecting color, contrast, edges, etc.

Further complexity arises from the various interconnections among bipolar cells, horizontal cells, and amacrine cells in the retina. The final result is differing populations of ganglion cells in the retina, a sub-population of which is also intrinsically photosensitive, using the photopigment melanopsin.

Ganglion cell (non-rod non-cone) photoreceptors

A non-rod non-cone photoreceptor in the eyes of mice, which was shown to mediate circadian rhythms, was discovered in 1991 by Foster et al.[2] These neuronal cells, called intrinsically photosensitive retinal ganglion cells (ipRGC), are a small subset (≈1–3%) of the retinal ganglion cells located in the inner retina, that is, in front[19] of the rods and cones located in the outer retina. These light sensitive neurons contain a photopigment, melanopsin,[20][21][22][23][24] which has an absorption peak of the light at a different wavelength (≈480 nm[25]) than rods and cones. Beside circadian / behavioral functions, ipRGCs have a role in initiating the pupillary light reflex.[26]

Dennis Dacey with colleagues showed in a species of Old World monkey that giant ganglion cells expressing melanopsin projected to the lateral geniculate nucleus (LGN).[27] Previously only projections to the midbrain (pre-tectal nucleus) and hypothalamus (suprachiasmatic nucleus) had been shown. However a visual role for the receptor was still unsuspected and unproven.

In 2007, Farhan H. Zaidi and colleagues published pioneering work using rodless coneless humans. Current Biology subsequently announced in their 2008 editorial, commentary and despatches to scientists and ophthalmologists, that the non-rod non-cone photoreceptor had been conclusively discovered in humans using landmark experiments on rodless coneless humans by Zaidi and colleagues[24][28][29][30] As had been found in other mammals, the identity of the non-rod non-cone photoreceptor in humans was found to be a ganglion cell in the inner retina. The workers had tracked down patients with rare diseases wiping out classic rod and cone photoreceptor function but preserving ganglion cell function.[28][29][30] Despite having no rods or cones the patients continued to exhibit circadian photoentrainment, circadian behavioural patterns, melanopsin suppression, and pupil reactions, with peak spectral sensitivities to environmental and experimental light matching that for the melanopsin photopigment. Their brains could also associate vision with light of this frequency.

In humans the retinal ganglion cell photoreceptor contributes to conscious sight as well as to non-image-forming functions like circadian rhythms, behaviour and pupil reactions.[31] Since these cells respond mostly to blue light, it has been suggested that they have a role in mesopic vision.[citation needed] Zaidi and colleagues' work with rodless coneless human subjects hence also opened the door into image-forming (visual) roles for the ganglion cell photoreceptor. It was discovered that there are parallel pathways for vision – one classic rod and cone-based pathway arising from the outer retina, and the other a rudimentary visual brightness detector pathway arising from the inner retina, which seems to be activated by light before the other.[31] Classic photoreceptors also feed into the novel photoreceptor system, and colour constancy may be an important role as suggested by Foster. The receptor could be instrumental in understanding many diseases including major causes of blindness worldwide like glaucoma, a disease that affects ganglion cells, and the study of the receptor offered potential as a new avenue to explore in trying to find treatments for blindness. It is in these discoveries of the novel photoreceptor in humans and in the receptor's role in vision, rather than its non-image-forming functions, where the receptor may have the greatest impact on society as a whole, though the impact of disturbed circadian rhythms is another area of relevance to clinical medicine.

Most work suggests that the peak spectral sensitivity of the receptor is between 460 and 482 nm. Steven Lockley et al. in 2003 showed that 460 nm wavelengths of light suppress melatonin twice as much as longer 555 nm light. However, in more recent work by Farhan Zaidi et al., using rodless coneless humans, it was found that what consciously led to light perception was a very intense 481 nm stimulus; this means that the receptor, in visual terms, enables some rudimentary vision maximally for blue light.[31]

See also


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External links

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