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Human eye cross-sectional view grayscale
Right human eye cross-sectional view. Courtesy NIH National Eye Institute. Many animals have eyes different from the human eye.
Latin '
Gray's subject #225 1014
MeSH A09.371.729


In vertebrate embryonic development, the retina and the optic nerve originate as outgrowths of the developing brain, so the retina is considered part of the central nervous system (CNS).[1]. It is the only part of the CNS that can be visualized non-invasively.



Anatomy of vertebrate retinaEdit


Section of retina.

The vertebrate retina has ten distinct layers.[2] From innermost to outermost, they include:

  1. Inner limiting membrane - Müller cell footplates
  2. Nerve fiber layer
  4. Inner plexiform layer
  5. Inner nuclear layer contains bipolar cells
  7. Outer nuclear layer
  8. External limiting membrane - Layer that separates the inner segment portions of the photoreceptors from their cell nucleaus.
  9. Photoreceptor layer - Rods / Cones
  10. Retinal pigment epithelium

Of these the four main layers of the ten, from outside in: pigment epithelium, the photoreceptor layer, bipolar cells, and finally, the ganglion cell layer.

Therefore, the optic nerve is less a nerve than a central tract, connecting the bipolars to the lateral geniculate body, a visual relay station in the diencephalon (the rear of the forebrain).[3]

Additional structures, not directly associated with vision, are found as outgrowths of the retina in some vertebrate groups. In birds, the pecten is a vascular structure of complex shape that projects from the retina into the vitreous humour; it supplies oxygen and nutrients to the eye, and may also aid in vision. Reptiles have a similar, but much simpler, structure, referred to as the papillary cone.[4]

Physical structure of human retinaEdit


Fig retine


In section the retina is no more than 0.5 mm thick. It has three layers of nerve cells and two of synapses, including the unique ribbon synapses. The optic nerve carries the ganglion cell axons to the brain and the blood vessels that open into the retina. The ganglion cells lie innermost in the retina while the photoreceptive cells lie outermost. Because of this counter-intuitive arrangement, light must first pass through and around the ganglion cells and through the thickness of the retina, (including its capillary vessels,not shown) before reaching the rods and cones. However it does not pass through the epithelium or the choroid (both of which are opaque).


Between the ganglion cell layer and the rods and cones there are two layers of neuropils where synaptic contacts are made. The neuropil layers are the outer plexiform layer and the inner plexiform layer. In the outer the rods and cones connect to the vertically running bipolar cells, and the horizontally oriented horizontal cells connect to ganglion cells.

The central retina is cone-dominated and the peripheral retina is rod-dominated. In total there are about seven million cones and a hundred million rods. At the centre of the macula is the foveal pit where the cones are smallest and in a hexagonal mosaic, the most efficient and highest density. Below the pit the other retina layers are displaced, before building up along the foveal slope until the rim of the fovea or parafovea which is the thickest portion of the retina. The macula has a yellow pigmentation from screening pigments and is known as the macula lutea. The area directly surrounding the fovea has the highest density of rods converging on single bipolars. Since the cones have a much lesser power of merging signals, the fovea allows for the sharpest vision the eye can attain.[1]

Since there are about 150 million receptors and only 1 million optic nerve fibers, and the horizontal action of the horizontal and amacrine cells can allow one area of the retina to control another (e.g., one stimulus inhibiting another), so the messages are merged and mixed. In some lower vertebrates, (e.g., the pigeon) there is a "centrifugal" control of messages, namely, that one layer could control another or higher regions of the brain can drive the retinal nerve cells, but in primates they are not existent.[1]

Vertebrate and cephalopod retina differencesEdit

The vertebrate retina is inverted in the sense that the light sensing cells sit at the back side of the retina, so that light has to pass through layers of neurons and capillaries before it reaches the rods and cones. By contrast, the cephalopod retina is in a more logical arrangement with the photoreceptors located at the front side of the retina, with processing neurons and capillaries behind them. Because of this, cephalopods do not have a blind spot.

The cephalopod retina does not originate as an outgrowth of the brain, as the vertebrate one does. It was originally argued that this difference shows that vertebrate and cephalopod eyes are not homologous but have evolved separately. The evolutionary biologist Richard Dawkins cites the imperfect structure of the human retina as confounding claims by creationists or intelligent design therorists that the human eye is so perfect it must have a designer.[5]

It has been recently anatomically shown in Zebrafish that though the inverted arranged is nonadaptive in creating avoidable scattering of light through tissue and so loss of light and image blur, it has space-saving advantages for small eyed animals in which there is a minimal vitreous body as the space between the lens and the photoreceptors’ light-sensitive outer segments is completely filled with retinal cells.[6]



The cones respond to bright light and mediate high-resolution colour vision during daylight illumination (also called "photopic" vision). The rods are saturated at daylight levels and don't contribute to pattern vision. However, rods do respond to dim light and mediate lower-resolution, monochromatic vision under very low levels of illumination (called "scotopic" vision). The illumination in most office settings falls between these two levels and is called "mesopic" vision. At these light levels, both the rods and cones are actively contributing pattern information to that exiting the eye. What contribution the rod information makes to pattern vision under these circumstances is unclear.

The response of cones to various wavelengths of light is called their "spectral sensitivity". In normal human vision, the spectral sensitivity of a cone falls into one of three subgroups. These are often called "red, green, and blue" cones but more accurately are short, medium, and long wavelength sensitive cone subgroups. It is a lack of one or more of the cone subtypes that causes individuals to have deficiencies in colour vision or various kinds of colour blindness. These individuals are not "blind" to objects of a particular colour but experience the inability to distinguish between two groups of colours that can be distinguished by people with normal vision. Humans have three different types of cones (trichromatic vision) while most other mammals lack cones with red sensitive pigment and therefore have poorer (dichromatic) colour vision. However, some animals have four spectral subgroups, e.g., the trout adds an ultraviolet subgroup to short, medium and long subgroups that are similar to humans. Some fish are sensitive to the polarization of light as well.






Spatial EncodingEdit

File:Receptive field.png


There are two types of center surround structures in the retina—on-centers and off-centers. On-centers have a positively weighted center and a negatively weighted surround. Off-centers are just the opposite. Positive weighting is more commonly known as excitatory and negative weighting is more commonly known as inhibitory.





-1/8 +1 -1/8





Simplified Signal Flow: Photoreceptors → Bipolar → Ganglion → Chiasm → LGN → V1 cortex

ERP - optic cabling

Diseases and disordersEdit

Main article: List of eye diseases and disorders


Diagnosis and treatmentEdit

A number of different instruments are available for the diagnosis of diseases and disorders affecting the retina. An ophthalmoscope is used to examine the retina. Recently, adaptive optics has been used to image individual rods and cones in the living human retina and a company based in Scotland have engineered technology that allows physicians to observe the complete retina without any discomfort to patients.[8]



Retinal blood supplyEdit

File:Fundus photograph-normal retina EDA06.JPG



A recent University of Pennsylvania study calculated the approximate bandwidth of human retinas is 8.75 megabits per second, whereas guinea pig retinas transfer at 875 kilobits.[9]

MacLaren & Pearson and colleagues at University College London and Moorfields Eye Hospital in London showed in 2006 that photoreceptor cells could be transplanted successfully in the mouse retina if donor cells were at a critical developmental stage.[10]. Recently Ader and colleagues in Dublin showed using the electron microscope that transplanted photoreceptors formed synaptic connections.[11].

Retinal gene therapyEdit

Gene therapy holds promise as a potential avenue to cure a wide range of retinal diseases. This involves using a non-infectious virus to shuttle a gene into a part of the retina. Recombinant adeno-associated virus (rAAV) vectors possess a number of features that render them ideally suited for retinal gene therapy, including a lack of pathogenicity, minimal immunogenicity, and the ability to transduce postmitotic cells in a stable and efficient manner.[12] rAAV vectors are increasingly utilized for their ability to mediate efficient transduction of retinal pigment epithelium (RPE), photoreceptor cells and retinal ganglion cells. Each cell type can be specifically targeted by choosing the appropriate combination of AAV serotype, promoter, and intraocular injection site.

The unique architecture of the retina and its relatively immune-privileged environment help this process. Tight junctions that form the blood retinal barrier separate the subretinal space from the blood supply, thus protecting it from microbes and most immune-mediated damage, and enhancing its potential to respond to vector-mediated therapies. The highly compartmentalized anatomy of the eye facilitates accurate delivery of therapeutic vector suspensions to specific tissues under direct visualization using microsurgical techniques.[13] In the sheltered environment of the retina, AAV vectors are able to maintain high levels of transgene expression in the retinal pigmented epithelium (RPE), photoreceptors, or ganglion cells for long periods of time after a single treatment. In addition, the eye and the visual system can be routinely and easily monitored for visual function and retinal structural changes after injections with noninvasive advanced technology, such as visual acuities, contrast sensitivity, fundus auto-fluorescence (FAF), dark-adapted visual thresholds, vascular diameters, pupillometry, electroretinography (ERG), multifocal ERG and optical coherence tomography (OCT).[14]

This strategy is effective against retinal diseases that have been studied including neovascular diseases that are features of age-related macular degeneration, diabetic retinopathy and retinopathy of prematurity. Since the regulation of vascularization in the mature retina involves a balance between endogenous positive growth factors, such as vascular endothelial growth factor (VEGF) and inhibitors of angiogenesis, such as pigment epithelium-derived factor (PEDF), rAAV-mediated expression of PEDF, angiostatin, and the soluble VEGF receptor sFlt-1, which are all antiangiogenic proteins, have been shown to reduce aberrant vessel formation in animal models.[15] Since specific gene therapies cannot readily be used to treat a significant fraction of patients with retinal dystrophy, there is a major interest in developing a more generally applicable survival factor therapy. Neurotrophic factors have the ability to modulate neuronal growth during development to maintain existing cells and to allow recovery of injured neuronal populations in the eye. AAV encoding neurotrophic factors such as fibroblast growth factor (FGF) family members and GDNF either protected photoreceptors from apoptosis or slowed down cell death.[15]

However, treatment of inherited retinal degenerative diseases such as retinitis pigmentosa and Leber congenital amaurosis (LCA) via gene replacement therapy constitutes the most straightforward and therefore the most promising approach for treating the autosomal recessive retinal disease. Leber Congenital Amaurosis (LCA2) is a defect of the RPE65 gene, which is responsible for the synthesis of 11-cis retinal, an important molecule in the visual phototransduction, and gene replacement therapy studies utilizing rpe65-encoding AAV have yielded hopeful results in animal models.[16] Based on several encouraging reports from animal models, at least three clinical trials are currently underway for the treatment of LCA using modified AAV vectors carrying the RPE65 cDNA and have reported positive preliminary results.[17]

See alsoEdit


  1. 1.0 1.1 1.2 "eye, human."Encyclopædia Britannica. 2008. Encyclopædia Britannica 2006 Ultimate Reference Suite DVD
  2. The Retinal Tunic
  4. Romer, Alfred Sherwood (1977). The Vertebrate Body, Philadelphia, PA: Holt-Saunders International.
  5. Dawkins, Richard (1986). The Blind Watchmaker, Longman. "An engineer would laugh at any suggestion that the photocells might point away from the light, with their wires departing on the side nearest the light. Yet this is what happens in all vertebrate retinas. The wire has to travel over the surface of the retina to a point where it dives through a hole in the retina, (the so-called blind spot) to joint the optic nerve. Light..has to pass through a forest of connecting wires, presumably suffering at least some attenuation and distortion....the principle of the thing would offend any tidy-minded engineer"
  6. Kröger RH, Biehlmaier O. (2009). Space-saving advantage of an inverted retina. Vision Res. 49(18):2318-21. PMID 19591859
  7. Oh, Kean, "Pathogenetic Mechanisms of Retinal Detachment", in Retina, ed. Ryan, S.J., Elsevier Health Sciences, Philadelphia, PA, 2006, p. 2013-2015
  8. Seeing into the Future Ingenia, March 2007
  9. Calculating the speed of sight - being-human - 28 July 2006 - New Scientist
  10. Retinal repair by transplantation of photoreceptor precursors : Abstract : Nature
  12. Astra Dinculescu, Lyudmyla Glushakova, Seok-Hong Min, William W. Hauswirth. Human Gene Therapy. June 2005, 16(6): 649-663.
  13. Enrico M. Curace, Alberto Auricchio. Versatility of AAV vectors for retinal gene transfer. Vision Research. 2008, 48:353-359.
  14. Anneke I. den Hollandera, Ronald Roepmana, Robert K. Koenekoopb, Frans P.M. Cremersa. Leber congenital amaurosis: Genes, proteins and disease mechanisms. Progress in Retinal and Eye Research. July 2008; 27(4):391-419.
  15. 15.0 15.1 Rolling F. Recombinant AAV-mediated gene transfer to the retina: gene therapy perspectives. Gene Therapy. 2004; 11: S26-S32.
  16. Tonia S. Rex. Rescue of Sight by Gene Therapy – Closer than It May Appear. Ophthalmic Genetics. 2007, 28:127-133.
  17. Xue Cai, Shannon M. Conley, Muna I Naash. RPE65: Role in the Visual Cycle, Human Retinal Disease, and Gene Therapy. Ophthalmic Genetics. June 2009, 30(2):57-62.

Further readingEdit

  • Meister M, Berry MJ (1999). The neural code of the retina. Neuron 22 (3): 435–50.
  • Rodieck RW (1965). Quantitative analysis of cat retinal ganglion cell response to visual stimuli. Vision Res. 5 (11): 583–601.
  • Wandell, Brian A. (1995). Foundations of vision, Sunderland, Mass: Sinauer Associates.
  • Schulz HL, Goetz T, Kaschkoetoe J, Weber BH (2004). The Retinome - defining a reference transcriptome of the adult mammalian retina/retinal pigment epithelium. BMC Genomics 5 (1): 50.

External linksEdit

Sensory system - Visual system - Eye - edit

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