How does the human eye function to process light and create visual perception. What are the key structures involved in eye physiology. How do rods and cones work together to enable vision in different light conditions. What is the role of photopigments in the visual process. How does the brain interpret signals from the eye to form images.

The Fundamental Structures of the Eye and Their Functions

The human eye is a marvel of biological engineering, comprised of several key structures that work in concert to enable vision. At the forefront is the cornea, a transparent layer that serves as the eye’s primary refractive surface. Behind it lies the iris, a muscular structure that controls the amount of light entering the eye by adjusting the size of the pupil. The lens, situated behind the iris, further focuses light onto the retina at the back of the eye.

The ciliary body, surrounding the lens, plays a crucial role in accommodation – the process of adjusting focus for objects at different distances. The choroid, a layer rich in blood vessels, nourishes the outer layers of the retina. Two fluid-filled chambers, containing aqueous humor anteriorly and vitreous humor posteriorly, help maintain the eye’s shape and internal pressure.

The Retina: The Eye’s Photosensitive Canvas

The retina is the light-sensitive layer at the back of the eye, containing millions of photoreceptor cells. These cells are responsible for converting light energy into electrical signals that can be interpreted by the brain. There are two main types of photoreceptors:

• Rods: Approximately 90 million in number, these cells are highly sensitive to light and are primarily responsible for vision in low-light conditions (scotopic vision).
• Cones: Numbering around 6 million, these cells are responsible for color vision and high visual acuity in bright light conditions (photopic vision).

The distribution of these cells across the retina is not uniform. The fovea, a small depression in the center of the retina, contains the highest concentration of cones and is responsible for our sharpest, most detailed vision. Rods, on the other hand, are more abundant in the peripheral retina, reaching their maximum density about 15 to 20 degrees from the fovea.

The Intricate Process of Light Perception

When light enters the eye, it undergoes a series of refractions as it passes through the cornea, aqueous humor, lens, and vitreous humor before reaching the retina. The lens, being flexible, can change its shape to focus on objects at varying distances – a process known as accommodation. This ability to adjust focus is what allows us to shift our gaze from nearby objects to those far away without losing clarity.

Once light reaches the retina, it triggers a complex cascade of events within the photoreceptor cells. This process, known as phototransduction, is what converts light energy into electrical signals that can be interpreted by the brain.

The Role of Photopigments in Vision

At the heart of the phototransduction process are photopigments – light-sensitive molecules found in the membranes of photoreceptor cells. In rod cells, this pigment is called rhodopsin, while cone cells contain different photopigments sensitive to different wavelengths of light.

Rhodopsin is a G-protein-coupled receptor composed of a protein called scotopsin and a vitamin A derivative called retinal. When light strikes rhodopsin, it causes a conformational change in the retinal molecule, initiating a cascade of biochemical reactions that ultimately lead to the generation of an electrical signal.

The Biochemistry of Vision: From Light to Electrical Signals

The process of converting light into electrical signals involves a complex series of biochemical reactions. When light activates rhodopsin, it triggers the activation of a G-protein called transducin. This, in turn, activates an enzyme called cGMP phosphodiesterase, which breaks down cyclic guanosine monophosphate (cGMP).

The reduction in cGMP levels causes ion channels in the cell membrane to close, leading to hyperpolarization of the rod cell. This change in electrical potential results in a decrease in the release of the neurotransmitter glutamate, which is interpreted by the brain as a light signal.

The Recovery Phase: Resetting the Visual Cycle

After light activation, the photoreceptor cells must return to their resting state to be ready for the next light stimulus. This recovery phase involves several proteins, including rhodopsin kinase, arrestin, and regulators of G protein signaling (RGS) proteins. These work together to inactivate rhodopsin and transducin, allowing the cell to reset its sensitivity to light.

Color Vision: The Interplay of Cone Photoreceptors

While rods are responsible for vision in low light conditions, cones are the primary cells responsible for color vision and high visual acuity in bright light. There are three types of cone cells, each sensitive to different wavelengths of light:

• S-cones: Sensitive to short wavelengths (blue light)
• M-cones: Sensitive to medium wavelengths (green light)
• L-cones: Sensitive to long wavelengths (red light)

The genes for these different cone types are located on different chromosomes. The S-cone photopigment gene is on chromosome 7, while the M-cone and L-cone genes are on the X chromosome. This genetic arrangement explains why color blindness is more common in males, as they only have one X chromosome.

The Trichromatic Theory of Color Vision

The presence of these three types of cones forms the basis of the trichromatic theory of color vision. According to this theory, our perception of color is based on the relative activation of these three cone types. For example, when we see yellow light, it activates both M-cones and L-cones, and our brain interprets this combination as the color yellow.

Visual Acuity and the Importance of the Fovea

Visual acuity, or the sharpness of vision, is highest at the fovea – a small, rod-free area of the retina densely packed with cones. This area is responsible for our central, most detailed vision. When we focus on an object, we instinctively move our eyes so that the image falls on the fovea, allowing us to see it in the greatest detail.

The high concentration of cones in the fovea is arranged in a specific pattern known as the “cone mosaic.” This arrangement allows for the highest possible resolution of visual information, enabling tasks such as reading fine print or recognizing facial features.

The Trade-off Between Sensitivity and Acuity

While the fovea provides the highest visual acuity, it’s not optimized for low-light vision. This is why we often find it difficult to see dim objects when looking directly at them. In low light conditions, our peripheral vision, which is rod-dominated, becomes more useful. This trade-off between sensitivity and acuity is a fundamental aspect of our visual system’s design.

The Visual Pathway: From Eye to Brain

Once the photoreceptor cells have converted light into electrical signals, this information needs to be transmitted to the brain for processing. This transmission occurs via the optic nerve, which carries visual information from the retina to various parts of the brain.

The visual information first reaches the lateral geniculate nucleus (LGN) in the thalamus, which acts as a relay station. From there, signals are sent to the primary visual cortex in the occipital lobe of the brain. This is where the initial processing of visual information occurs, including the detection of edges, orientations, and basic shapes.

Higher-Order Visual Processing

From the primary visual cortex, information is distributed to various other areas of the brain for more complex processing. These include:

• The ventral stream: Often called the “what” pathway, this processes information about object recognition and form representation.
• The dorsal stream: Known as the “where” pathway, this is involved in spatial awareness and guidance of actions.

Through these pathways, our brain integrates the raw visual data with other sensory inputs and cognitive processes to create our rich, detailed perception of the world around us.

Adaptations for Different Light Conditions

Our visual system has remarkable adaptability, allowing us to see in a wide range of light conditions, from bright sunlight to near darkness. This adaptability is achieved through several mechanisms:

Light and Dark Adaptation

When we move from a bright environment to a dark one, our eyes undergo a process called dark adaptation. This involves several changes:

1. Pupil dilation: The iris muscles relax, allowing the pupil to expand and let in more light.
2. Rod cell activation: As light levels decrease, rod cells become more active, taking over from cone cells.
3. Rhodopsin regeneration: In darkness, rhodopsin molecules that were bleached by light are regenerated, increasing light sensitivity.

The reverse process, light adaptation, occurs when we move from darkness to light. This involves pupil constriction and a shift from rod-dominated to cone-dominated vision.

The Role of Vitamin A in Vision

Vitamin A plays a crucial role in vision, particularly in low-light conditions. It’s a key component of rhodopsin, the photopigment in rod cells. A deficiency in vitamin A can lead to night blindness, a condition where a person has difficulty seeing in low light.

The visual cycle, which regenerates rhodopsin after light exposure, relies on a continuous supply of vitamin A. This underscores the importance of maintaining adequate vitamin A levels through a balanced diet or supplementation when necessary.

Common Visual Disorders and Their Physiological Basis

Understanding the physiology of the eye provides insight into various visual disorders. Here are some common conditions and their underlying physiological causes:

Myopia (Nearsightedness)

In myopia, the eye focuses images in front of the retina instead of directly on it. This can be due to an elongated eyeball or an overly curved cornea. As a result, distant objects appear blurry while close objects remain clear.

Hyperopia (Farsightedness)

Hyperopia is the opposite of myopia. Here, the eye focuses images behind the retina, making nearby objects appear blurry. This can be due to a shorter than normal eyeball or a flatter cornea.

Astigmatism

Astigmatism occurs when the cornea or lens has an irregular shape, causing light to focus on multiple points on the retina instead of a single point. This results in blurred or distorted vision at all distances.

Color Blindness

Color blindness typically results from a genetic defect that affects the function or presence of certain cone cells. The most common form is red-green color blindness, which is more prevalent in males due to the location of the relevant genes on the X chromosome.

Age-Related Macular Degeneration (AMD)

AMD affects the macula, the central part of the retina responsible for sharp, detailed vision. It can be caused by the accumulation of cellular debris (dry AMD) or abnormal blood vessel growth (wet AMD) in the macula.

Understanding these disorders in terms of eye physiology not only helps in diagnosis but also guides the development of treatments and preventive measures.

Physiology, Eye – StatPearls – NCBI Bookshelf

Parker E. Ludwig; Rishita Jessu; Craig N. Czyz.

Author Information and Affiliations

Last Update: October 7, 2022.

Introduction

The proper function of the eye depends on its ability to receive and process energy from light in the environment, produce action potentials in specialized nerve cells, and relay those potentials through the optic nerve (cranial nerve II) to the brain. The cornea, iris, ciliary body, and lens all play a role in transmitting and focusing light onto the sensory component of the eye, the retina. Structures such as the choroid, aqueous and vitreous humor, and the lacrimal system are important for physiological balance, appropriate pressure maintenance, and nourishment of ocular tissues.[1]

Issues of Concern

Visual acuity relies on proper refraction or bending of light passing through structures of varying densities as the light is transmitted through the cornea, aqueous humor, lens, and vitreous humor before striking the retina. The lens is the adjustable component of the refractive system: its shape is altered by the contraction or relaxation of the ciliary muscle to focus on objects that are near or far.

Cellular Level

The retina is comprised of two types of photoreceptor cells: rods and cones. Rods are the cells primarily responsible for scotopic vision, or low-light vision. Rods are the more abundant cell-type of the retina and reach their maximum density approximately 15 to 20 degrees from the fovea, a small depression in the retina of the eye where visual acuity is highest. There are approximately 90 million rod cells in the human retina. The cones confer color vision and high spatial acuity and are the cell-type most activated at higher light levels when photopic vision predominates. The fovea has the highest density of cones and is free of rods. The human retina contains approximately 6 million cone cells. It should be noted that there is a visual field “blind spot” at the site of the optic nerve where photoreceptor cells are absent.

In comparing the photoreceptor cell types, rods have more photopigment and exhibit high amplification, highly convergent retinal pathways, and high sensitivity, while cones have a faster response with short integration times, are directionally selective, and exhibit high acuity. The term “bleaching” refers to the absorption of a photon by a pigment molecule. Rods are achromatic, meaning they contain one type of pigment, while cones are arranged in a chromatic organization of three different pigments. In the fovea, this arrangement takes on the form of what is referred to as the “cone mosaic.” Photopigment molecules are embedded in the membranes of photoreceptors.[1][2][3]

Mechanism

The photopigment in rods is called rhodopsin. Human rhodopsin is a G-protein-coupled receptor made up of 348 amino acids arranged in seven transmembrane domains, and its gene is located on chromosome 3. Rhodopsin consists of a protein called scotopsin and its covalently-bound cofactor, retinal. The chromophore retinal lies in a pocket formed by the transmembrane domains of scotopsin. Retinal is a vitamin A derivative produced from dietary beta-carotene. Inactive, retinal exists in the 11-cis-retinal conformation. Upon exposure to light, retinal is isomerized to all-trans-retinal leading to a series of changes in conformation to the form metarhodopsin II (Meta II). Meta II activates the G protein transducin, after which its alpha subunit is released. The transducin alpha subunit, bound to guanosine triphosphate (GTP), then activates cyclic guanosine monophosphate (cGMP) phosphodiesterase.  cGMP is hydrolyzed by cGMP phosphodiesterase which inhibits its activation of cGMP-dependent cation channels and causes hyperpolarization of the rod cell and consequent release of glutamate which depolarizes some neurons and hyperpolarizes others. Reversion of rods to their resting state involves rhodopsin kinase (RK), arrestin, a regulator of G protein signaling (RGS) protein, and closure of cGMP channels. The activity of transducin is partially inhibited by the phosphorylation of the rhodopsin cytosolic tail by RK. Arrestin then binds the phosphorylated rhodopsin to inactivate it further. The RGS protein increases the rate of GTP to GDP hydrolysis to convert transducin into its “off” state. cGMP-sensitive channel closure decreases the concentration of calcium ions, which stimulates calcium ion-sensitive proteins to activate guanylyl cyclase causing restoration of cGMP levels and plasma membrane depolarization.

In contrast to rods, there are three different types of cones: S-cones (short wavelength-sensitive), M-cones (medium wavelength-sensitive), and L-cones (long wavelength-sensitive). The S-cone photopigment gene is encoded on chromosome 7, while those of the M-cones and L-cones are on the X chromosome. All cone receptors contain the protein photopsin in modified conformations to enable activation by different wavelengths of light. The different types of photopsin, which are also opsins combined with retinal, are the cone equivalent of rhodopsin in rods. The absorption maxima for photopsin I, photopsin II, and photopsin III are for yellowish-green, green, and bluish-violet light respectively. The increased visual acuity associated with cones is due to their individual connections to the optic nerve, which enables improved distinction between isolated signals. As compared to rods, each step in the generation of a response to light in cones is less effective, and the reactions responsible for termination of such a light response are faster. Melanopsin is located in some ganglion cells of the retina and is responsible for non-visual responses to light such as the regulation of circadian rhythms and the pupillary reflex. The function of melanopsin is similar to that of invertebrate opsins, it absorbs light and triggers a cascade that allows the brain to generate and modify the body’s circadian rhythm. The absorption of blue light by melanopsin can disrupt the body’s circadian rhythm and can lead to insomnia. 

Signals from photoreceptor cells are transmitted through bipolar cells to the retinal ganglion cells (RGCs) in the innermost layer of the retina, which carry the signals through the optic nerve (composed of bundled RGC axons) to the brain. Retinal horizontal cells are responsible for providing inhibitory feedback to photoreceptor cells. It is interesting to note that light exposure has an inhibitory effect on photoreceptor neurotransmitter release; glutamate is released in states of darkness, causing depolarization of the membrane at rest, and its release is inhibited by photon absorption.[4][5][6][7][8]

Clinical Significance

Astigmatism refers to a blurring of vision due to the irregular curvature of the cornea or the lens. Compensation for such abnormalities is generally made through the use of extraocular lenses such as glasses or contact lenses, or refractive surgery. Myopia or nearsightedness is the result of an excessively long eyeball or thick lens. Hyperopia or farsightedness typically is due to an abnormally short globe or thin lens. Both types of visual disturbance are corrected using intra- or extraocular lenses and/or refractive surgery.

Glaucoma refers to a group of diseases that cause optic nerve damage due to increased intraocular pressure. Open-angle glaucoma is the most common type and is characterized by a normal angle between the iris and cornea (iridocorneal angle). Other types of glaucoma include closed-angle and normal-tension glaucoma. While some cases of glaucoma result from mutations of certain genes, the cause of primary glaucoma remain largely unknown. Glaucoma is usually associated with either an overproduction of aqueous humor or impairment in the drainage of aqueous.

Achromatopsia describes a partial or total absence of color vision. Usually, it is inherited in an autosomal recessive manner. Genetic mutations, most commonly in CNGA3, CNGB3, GNAT2, PDE6C, or PDE6H, cause inappropriate responses of cones to light exposure. This can mean a complete lack of functionality or a significant deficit.

Some of the most common retinal diseases include diabetic retinopathy (DR), and age-related macular degeneration (AMD). AMD exits in two forms: dry (atrophic) and wet (exudative or neovascular). In the majority of people, AMD starts as the dry form and in some individuals, it progresses to the wet type (15% to 20%). AMD is always bilateral, but not always the same form in both eyes. Also, the disease does not necessarily progress at the same rate in both eyes. Both AMD and DR involve degeneration of retinal structure which leads to disruption of the phototransduction pathway discussed. In diabetic retinopathy, blood vessels and neurons are damaged by an overaccumulation of glucose, and in severe disease, the proliferation of new blood vessels can further exacerbate visual impairments. In AMD, there is a buildup of damaged cellular components such as lipofuscin (intracellular) and drusen (extracellular). This leads to damage to the macula which causes dysfunctional central vision and can ultimately lead to complete blindness. Choroidal neovascularization can also exacerbate AMD. Many different genes have been implicated in the development and progression of AMD.

In contrast to achromatopsia, retinitis pigmentosa (RP) affects the rod cells of the retina. Rods are progressively lost as the disease advances, leading to difficulty seeing at night, and decreased peripheral vision which has been described as “tunnel vision”. Symptoms often begin in childhood and progressively worsen with age. Mutations in many genes have been shown to cause RP, with possible inheritance patterns including autosomal dominant, autosomal recessive, X-linked, and mitochondrial inheritance.[9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24]

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Figure

Schematic diagram of the human eye. Contributed by the Public Domain

References

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Kawamura S, Tachibanaki S. Rod and cone photoreceptors: molecular basis of the difference in their physiology. Comp Biochem Physiol A Mol Integr Physiol. 2008 Aug;150(4):369-77. [PubMed: 18514002]

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Mendez A, Burns ME, Roca A, Lem J, Wu LW, Simon MI, Baylor DA, Chen J. Rapid and reproducible deactivation of rhodopsin requires multiple phosphorylation sites. Neuron. 2000 Oct;28(1):153-64. [PubMed: 11086991]

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Zhang TZ, Fan B, Chen X, Wang WJ, Jiao YY, Su GF, Li GY. Suppressing autophagy protects photoreceptor cells from light-induced injury. Biochem Biophys Res Commun. 2014 Jul 25;450(2):966-72. [PubMed: 24971547]

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Lamb TD, Hunt DM. Evolution of the vertebrate phototransduction cascade activation steps. Dev Biol. 2017 Nov 01;431(1):77-92. [PubMed: 28347645]

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Astakhova L, Firsov M, Govardovskii V. Activation and quenching of the phototransduction cascade in retinal cones as inferred from electrophysiology and mathematical modeling. Mol Vis. 2015;21:244-63. [PMC free article: PMC4392649] [PubMed: 25866462]

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Chen CK. RGS Protein Regulation of Phototransduction. Prog Mol Biol Transl Sci. 2015;133:31-45. [PMC free article: PMC4664578] [PubMed: 26123301]

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Zhou Z, Doggett TA, Sene A, Apte RS, Ferguson TA. Autophagy supports survival and phototransduction protein levels in rod photoreceptors. Cell Death Differ. 2015 Mar;22(3):488-98. [PMC free article: PMC4326583] [PubMed: 25571975]

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Emanuel AJ, Do MT. Melanopsin tristability for sustained and broadband phototransduction. Neuron. 2015 Mar 04;85(5):1043-55. [PMC free article: PMC4351474] [PubMed: 25741728]

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Schön C, Sothilingam V, Mühlfriedel R, Garcia Garrido M, Beck SC, Tanimoto N, Wissinger B, Paquet-Durand F, Biel M, Michalakis S, Seeliger MW. Gene Therapy Successfully Delays Degeneration in a Mouse Model of PDE6A-Linked Retinitis Pigmentosa (RP43). Hum Gene Ther. 2017 Dec;28(12):1180-1188. [PubMed: 29212391]

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Occelli LM, Schön C, Seeliger MW, Biel M, Michalakis S, Petersen-Jones SM. Gene Supplementation Rescues Rod Function and Preserves Photoreceptor and Retinal Morphology in Dogs, Leading the Way Toward Treating Human PDE6A-Retinitis Pigmentosa. Hum Gene Ther. 2017 Dec;28(12):1189-1201. [PubMed: 29212382]

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Eblimit A, Agrawal SA, Thomas K, Anastassov IA, Abulikemu T, Moayedi Y, Mardon G, Chen R. Conditional loss of Spata7 in photoreceptors causes progressive retinal degeneration in mice. Exp Eye Res. 2018 Jan;166:120-130. [PMC free article: PMC5756513] [PubMed: 29100828]

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Wong WL, Su X, Li X, Cheung CM, Klein R, Cheng CY, Wong TY. Global prevalence of age-related macular degeneration and disease burden projection for 2020 and 2040: a systematic review and meta-analysis. Lancet Glob Health. 2014 Feb;2(2):e106-16. [PubMed: 25104651]

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Mehta S. Age-Related Macular Degeneration. Prim Care. 2015 Sep;42(3):377-91. [PubMed: 26319344]

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Gahlaut N, Suarez S, Uddin MI, Gordon AY, Evans SM, Jayagopal A. Nanoengineering of therapeutics for retinal vascular disease. Eur J Pharm Biopharm. 2015 Sep;95(Pt B):323-30. [PMC free article: PMC4604030] [PubMed: 26022642]

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Jenkins AJ, Joglekar MV, Hardikar AA, Keech AC, O’Neal DN, Januszewski AS. Biomarkers in Diabetic Retinopathy. Rev Diabet Stud. 2015 Spring-Summer;12(1-2):159-95. [PMC free article: PMC5397989] [PubMed: 26676667]

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Disclosure: Parker Ludwig declares no relevant financial relationships with ineligible companies.

Disclosure: Rishita Jessu declares no relevant financial relationships with ineligible companies.

Disclosure: Craig Czyz declares no relevant financial relationships with ineligible companies.

Physiology, Eye – StatPearls – NCBI Bookshelf

Parker E. Ludwig; Rishita Jessu; Craig N. Czyz.

Author Information and Affiliations

Last Update: October 7, 2022.

Introduction

The proper function of the eye depends on its ability to receive and process energy from light in the environment, produce action potentials in specialized nerve cells, and relay those potentials through the optic nerve (cranial nerve II) to the brain. The cornea, iris, ciliary body, and lens all play a role in transmitting and focusing light onto the sensory component of the eye, the retina. Structures such as the choroid, aqueous and vitreous humor, and the lacrimal system are important for physiological balance, appropriate pressure maintenance, and nourishment of ocular tissues. [1]

Issues of Concern

Visual acuity relies on proper refraction or bending of light passing through structures of varying densities as the light is transmitted through the cornea, aqueous humor, lens, and vitreous humor before striking the retina. The lens is the adjustable component of the refractive system: its shape is altered by the contraction or relaxation of the ciliary muscle to focus on objects that are near or far.

Cellular Level

The retina is comprised of two types of photoreceptor cells: rods and cones. Rods are the cells primarily responsible for scotopic vision, or low-light vision. Rods are the more abundant cell-type of the retina and reach their maximum density approximately 15 to 20 degrees from the fovea, a small depression in the retina of the eye where visual acuity is highest. There are approximately 90 million rod cells in the human retina. The cones confer color vision and high spatial acuity and are the cell-type most activated at higher light levels when photopic vision predominates. The fovea has the highest density of cones and is free of rods. The human retina contains approximately 6 million cone cells. It should be noted that there is a visual field “blind spot” at the site of the optic nerve where photoreceptor cells are absent.

In comparing the photoreceptor cell types, rods have more photopigment and exhibit high amplification, highly convergent retinal pathways, and high sensitivity, while cones have a faster response with short integration times, are directionally selective, and exhibit high acuity. The term “bleaching” refers to the absorption of a photon by a pigment molecule. Rods are achromatic, meaning they contain one type of pigment, while cones are arranged in a chromatic organization of three different pigments. In the fovea, this arrangement takes on the form of what is referred to as the “cone mosaic.” Photopigment molecules are embedded in the membranes of photoreceptors.[1][2][3]

Mechanism

The photopigment in rods is called rhodopsin. Human rhodopsin is a G-protein-coupled receptor made up of 348 amino acids arranged in seven transmembrane domains, and its gene is located on chromosome 3. Rhodopsin consists of a protein called scotopsin and its covalently-bound cofactor, retinal. The chromophore retinal lies in a pocket formed by the transmembrane domains of scotopsin. Retinal is a vitamin A derivative produced from dietary beta-carotene. Inactive, retinal exists in the 11-cis-retinal conformation. Upon exposure to light, retinal is isomerized to all-trans-retinal leading to a series of changes in conformation to the form metarhodopsin II (Meta II). Meta II activates the G protein transducin, after which its alpha subunit is released. The transducin alpha subunit, bound to guanosine triphosphate (GTP), then activates cyclic guanosine monophosphate (cGMP) phosphodiesterase.  cGMP is hydrolyzed by cGMP phosphodiesterase which inhibits its activation of cGMP-dependent cation channels and causes hyperpolarization of the rod cell and consequent release of glutamate which depolarizes some neurons and hyperpolarizes others. Reversion of rods to their resting state involves rhodopsin kinase (RK), arrestin, a regulator of G protein signaling (RGS) protein, and closure of cGMP channels. The activity of transducin is partially inhibited by the phosphorylation of the rhodopsin cytosolic tail by RK. Arrestin then binds the phosphorylated rhodopsin to inactivate it further. The RGS protein increases the rate of GTP to GDP hydrolysis to convert transducin into its “off” state. cGMP-sensitive channel closure decreases the concentration of calcium ions, which stimulates calcium ion-sensitive proteins to activate guanylyl cyclase causing restoration of cGMP levels and plasma membrane depolarization.

In contrast to rods, there are three different types of cones: S-cones (short wavelength-sensitive), M-cones (medium wavelength-sensitive), and L-cones (long wavelength-sensitive). The S-cone photopigment gene is encoded on chromosome 7, while those of the M-cones and L-cones are on the X chromosome. All cone receptors contain the protein photopsin in modified conformations to enable activation by different wavelengths of light. The different types of photopsin, which are also opsins combined with retinal, are the cone equivalent of rhodopsin in rods. The absorption maxima for photopsin I, photopsin II, and photopsin III are for yellowish-green, green, and bluish-violet light respectively. The increased visual acuity associated with cones is due to their individual connections to the optic nerve, which enables improved distinction between isolated signals. As compared to rods, each step in the generation of a response to light in cones is less effective, and the reactions responsible for termination of such a light response are faster. Melanopsin is located in some ganglion cells of the retina and is responsible for non-visual responses to light such as the regulation of circadian rhythms and the pupillary reflex. The function of melanopsin is similar to that of invertebrate opsins, it absorbs light and triggers a cascade that allows the brain to generate and modify the body’s circadian rhythm. The absorption of blue light by melanopsin can disrupt the body’s circadian rhythm and can lead to insomnia.  

Signals from photoreceptor cells are transmitted through bipolar cells to the retinal ganglion cells (RGCs) in the innermost layer of the retina, which carry the signals through the optic nerve (composed of bundled RGC axons) to the brain. Retinal horizontal cells are responsible for providing inhibitory feedback to photoreceptor cells. It is interesting to note that light exposure has an inhibitory effect on photoreceptor neurotransmitter release; glutamate is released in states of darkness, causing depolarization of the membrane at rest, and its release is inhibited by photon absorption.[4][5][6][7][8]

Clinical Significance

Astigmatism refers to a blurring of vision due to the irregular curvature of the cornea or the lens. Compensation for such abnormalities is generally made through the use of extraocular lenses such as glasses or contact lenses, or refractive surgery. Myopia or nearsightedness is the result of an excessively long eyeball or thick lens. Hyperopia or farsightedness typically is due to an abnormally short globe or thin lens. Both types of visual disturbance are corrected using intra- or extraocular lenses and/or refractive surgery.

Glaucoma refers to a group of diseases that cause optic nerve damage due to increased intraocular pressure. Open-angle glaucoma is the most common type and is characterized by a normal angle between the iris and cornea (iridocorneal angle). Other types of glaucoma include closed-angle and normal-tension glaucoma. While some cases of glaucoma result from mutations of certain genes, the cause of primary glaucoma remain largely unknown. Glaucoma is usually associated with either an overproduction of aqueous humor or impairment in the drainage of aqueous.

Achromatopsia describes a partial or total absence of color vision. Usually, it is inherited in an autosomal recessive manner. Genetic mutations, most commonly in CNGA3, CNGB3, GNAT2, PDE6C, or PDE6H, cause inappropriate responses of cones to light exposure. This can mean a complete lack of functionality or a significant deficit.

Some of the most common retinal diseases include diabetic retinopathy (DR), and age-related macular degeneration (AMD). AMD exits in two forms: dry (atrophic) and wet (exudative or neovascular). In the majority of people, AMD starts as the dry form and in some individuals, it progresses to the wet type (15% to 20%). AMD is always bilateral, but not always the same form in both eyes. Also, the disease does not necessarily progress at the same rate in both eyes. Both AMD and DR involve degeneration of retinal structure which leads to disruption of the phototransduction pathway discussed. In diabetic retinopathy, blood vessels and neurons are damaged by an overaccumulation of glucose, and in severe disease, the proliferation of new blood vessels can further exacerbate visual impairments. In AMD, there is a buildup of damaged cellular components such as lipofuscin (intracellular) and drusen (extracellular). This leads to damage to the macula which causes dysfunctional central vision and can ultimately lead to complete blindness.  Choroidal neovascularization can also exacerbate AMD. Many different genes have been implicated in the development and progression of AMD.

In contrast to achromatopsia, retinitis pigmentosa (RP) affects the rod cells of the retina. Rods are progressively lost as the disease advances, leading to difficulty seeing at night, and decreased peripheral vision which has been described as “tunnel vision”. Symptoms often begin in childhood and progressively worsen with age. Mutations in many genes have been shown to cause RP, with possible inheritance patterns including autosomal dominant, autosomal recessive, X-linked, and mitochondrial inheritance.[9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24]

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Figure

Schematic diagram of the human eye. Contributed by the Public Domain

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Disclosure: Parker Ludwig declares no relevant financial relationships with ineligible companies.

Disclosure: Rishita Jessu declares no relevant financial relationships with ineligible companies.

Disclosure: Craig Czyz declares no relevant financial relationships with ineligible companies.

The structure and functions of the eye, the anatomy of the eye

A person sees not through the eyes, but through the eyes, from where information is transmitted through the optic nerve, chiasm, visual tracts to certain areas of the occipital lobes of the cerebral cortex, where the picture of the external world that we see is formed. All these organs make up our visual analyzer or visual system.

The presence of two eyes allows us to make our vision stereoscopic (that is, to form a three-dimensional image). The right side of the retina of each eye transmits the “right side” of the image through the optic nerve to the right side of the brain, the left side of the retina does the same. Then the two parts of the image – the right and the left – the brain connects together.

Since each eye perceives “its own” picture, if the joint movement of the right and left eyes is disturbed, binocular vision may be disturbed. Simply put, you will start seeing double or you will see two completely different pictures at the same time.

Basic functions of the eye

• optical system that projects an image;
• system that perceives and “codes” the received information for the brain;
• “service” life support system.

Structure of the eye

The eye can be called a complex optical device. Its main task is to “transmit” the correct image to the optic nerve.

Cornea is the transparent membrane covering the front of the eye. There are no blood vessels in it, it has a large refractive power. Enters the optical system of the eye. The cornea borders on the opaque outer shell of the eye – the sclera. See the structure of the cornea.

Anterior chamber is the space between the cornea and the iris. It is filled with intraocular fluid.

Iris – similar in shape to a circle with a hole inside (pupil). The iris consists of muscles, with the contraction and relaxation of which the size of the pupil changes. It enters the choroid of the eye. The iris is responsible for the color of the eyes (if it is blue, it means that there are few pigment cells in it, if it is brown, there are many). Performs the same function as the aperture in a camera, adjusting the light output.

Pupil – hole in the iris. Its dimensions usually depend on the level of illumination. The more light, the smaller the pupil.

Lens is the “natural lens” of the eye. It is transparent, elastic – it can change its shape, “focusing” almost instantly, due to which a person sees well both near and far. Encapsulated, held in place by eyelash band . The lens, like the cornea, is part of the optical system of the eye.

Vitreous body is a gel-like transparent substance located in the back of the eye. The vitreous body maintains the shape of the eyeball and is involved in intraocular metabolism. Enters the optical system of the eye.

Retina – consists of photoreceptors (they are sensitive to light) and nerve cells. Receptor cells located in the retina are divided into two types: cones and rods. In these cells, which produce the enzyme rhodopsin, the energy of light (photons) is converted into electrical energy of the nervous tissue, i. e., a photochemical reaction.

The sticks are highly light sensitive and allow you to see in poor light, they are also responsible for peripheral vision. Cones, on the contrary, require more light for their work, but it is they that allow you to see fine details (responsible for central vision), make it possible to distinguish colors. The largest accumulation of cones is in the fovea centralis (macula), which is responsible for the highest visual acuity. The retina is adjacent to the choroid, but loosely in many areas. This is where it tends to flake off in various retinal diseases.

Sclera is the opaque outer shell of the eyeball, which passes into the transparent cornea in the anterior part of the eyeball. 6 oculomotor muscles are attached to the sclera. It contains a small number of nerve endings and blood vessels.

Choroid – lines the posterior sclera, adjacent to the retina, with which it is closely connected. The choroid is responsible for the blood supply to the intraocular structures. In diseases of the retina, it is very often involved in the pathological process. There are no nerve endings in the choroid, therefore, when it is ill, pain does not occur, usually signaling some kind of malfunction.

Optic nerve – with the help of the optic nerve, signals from the nerve endings are transmitted to the brain.

Useful reading

General questions about treatment in the clinic

The structure and functions of the human eye

The structure and functions of the human eye

The human eye is an organ with a complex structure that allows us to receive almost 90% of information about the world. Its main task is to “transmit” the correct image to the optic nerve. The eye has a special structure, unlike other organs: it consists of peripheral, conductive and central parts. Each of its parts, each layer has its own functions, properties and purpose.

Structure of the eye

The eyeballs are located in the sockets, which reliably protect them from various injuries. The movement of the “apples” occurs due to six external muscles, which are attached to the sclera and bone tissue. The surface of the organ is regularly moistened thanks to the tears that are produced by the lacrimal gland and form a special film that creates a barrier to protect against external factors. The front of the eye is also protected by the eyelids, which prevent large amounts of germs, dust and pollution from entering it.

Shells

The eyeball has several shells, each of which has a specific function:

1. Conjunctiva. Completely transparent outer shell allowing normal eyeball movement.
2. Fibrous. It mainly consists of the sclera – a dense layer that provides protection to the organ and performs a supporting function. The anterior part of the fibrous membrane is called the cornea – this is its most sensitive area, which is the optical refractive medium.
3. Vascular. This shell provides normal blood supply to the organ of vision and trophism of the structures located inside the eye.
4. Mesh. This is the inner sheath, which is a multi-layered tissue made up of nerves. The macula is located in the retina and is responsible for central vision.

The choroid, in turn, also consists of several elements:

1. Choroid – performs a trophic function, closely contacts with the retina and sclera.
2. Ciliary body is a neuromuscular element that contributes to the natural hydration of the organ.
3. Iris is the element responsible for the color of the eyes. In the center of the iris is the pupil, which limits the amount of light rays perceived by a person.

Chambers

The eyeball has two fluid-filled chambers that are normally closely connected to each other through the pupil. Their main task is to bring the intraocular tissues to a normal state and participate in the conduction of light rays to the retina. The anterior chamber is located directly behind the cornea, while the posterior chamber is located behind the iris. Due to the regular formation and outflow of fluid, both chambers have the same volume. The formation of fluid occurs in the posterior chamber, and then it flows into the drainage system located in the anterior.

Optical structures

The eye perceives objects with the help of optical structures that react to the image and conduct light rays. The quality of vision depends on the state of these structures.

1. The cornea is essentially a lens that is responsible for the transmission and refraction of light rays.
2. Lens focuses light rays and is responsible for their transformation into a nerve impulse.
3. Aqueous humor and vitreous body also have refractive properties. The quality of vision depends on their transparency (or vice versa, cloudiness), that is, how clear a person sees the outlines of objects.

Basic functions

1. Central vision. The task of this function is to perceive small objects and details. It is by this indicator that ophthalmologists determine the overall visual acuity. For diagnostics, a special table with graphic elements of different sizes is used.
2. Peripheral . Forms a field visible to the eye with a constant direction of view. With the help of this function, a person can navigate in space, as well as see objects that fall into the extreme coverage areas.
3. Color . This is the ability of the organ of vision to perceive different colors and shades. Colors are divided according to the wavelength of radiation and are long-wave (shades of the red spectrum), medium-wave (green-yellow spectrum) and short-wave (violet, cyan, blue). If the eye normally perceives all three spectra, then it is able to perceive many intermediate shades that arise when the three primary colors are mixed.
4. Light perception . This function allows you to perceive and distinguish the brightness of the rays of light. Violation of light perception is a pathology and can be an early sign of various diseases.
5. Binocular . Binocular vision is responsible for the clear perception of one object with both eyes at once. This function works thanks to the cortical section of the analyzer.

Binocular function is fully developed by 6–15 years of age. In order for binocular vision to develop correctly, the following conditions must be met:

• symmetrical arrangement of the organs of vision;
• free movement of the oculomotor muscles – with normal muscle tone, a parallel arrangement of the visual axes should be ensured when the rays are projected onto the central region of the retina;
• equal value of the object in question in both organs;
• normal functioning of the retina, optic nerve and pathways.

To make sure that all visual functions develop correctly, it is important to see an ophthalmologist regularly from an early age. The doctor will monitor the development of visual functions and, if necessary, make timely corrections to avoid the development of pathologies.

Why the correct performance of visual functions is impaired

There are several factors that can have a negative impact on the work of visual functions:

1. Lack of regular consultations with an ophthalmologist . Vision should be checked once a year in order to prevent the development of diseases in time or to evaluate the effectiveness of the treatment.
2. Incorrect use or incorrect fitting of contact lenses. Do not sleep in the lenses, and do not walk in them for longer than indicated in the instructions for each model. Also, you can’t choose the means of correction on your own – this can only be done according to the prescription of an ophthalmologist. At least once a year, you need to undergo a re-diagnosis in order to change lenses in time if visual acuity has changed.
3. Incorrect light distribution. High-quality lighting while reading, drawing and any other work is very important for eye health.
4. No sunglasses.