Eyes physiology. Eye Physiology: Understanding the Intricate Workings of Human Vision

28.11.202010.07.2023 by alexxlab

How does the human eye function to process light and create vision. What are the key structures involved in visual perception. How do rods and cones in the retina contribute to sight. What is the biochemical process behind light detection in photoreceptor cells. How does the eye adapt to different light conditions.

Содержание

The Fundamental Structures and Functions of the Human Eye

The human eye is a remarkable organ that allows us to perceive the visual world around us. Its proper function relies on a complex interplay of various structures working in harmony to receive, process, and transmit visual information to the brain. Let’s explore the key components and their roles in vision:

Cornea: The clear, dome-shaped surface that covers the front of the eye
Iris: The colored part of the eye that controls the amount of light entering
Ciliary body: A structure that controls the shape of the lens
Lens: The transparent structure that focuses light onto the retina
Retina: The light-sensitive layer at the back of the eye
Optic nerve: The pathway that carries visual information to the brain

These structures work together to enable the eye to capture light energy from the environment, convert it into electrical signals, and relay those signals to the brain for interpretation. The process of vision begins when light enters the eye through the cornea, passes through the pupil (controlled by the iris), and is focused by the lens onto the retina.

The Role of Supporting Structures in Ocular Health

While the primary components of the eye are crucial for vision, several supporting structures play vital roles in maintaining ocular health and function:

Choroid: A layer of blood vessels that nourishes the outer layers of the retina
Aqueous humor: The clear fluid in the front part of the eye that maintains intraocular pressure
Vitreous humor: The gel-like substance that fills the back of the eye and helps maintain its shape
Lacrimal system: The tear-producing and draining structures that keep the eye lubricated and clean

These supporting structures ensure that the eye remains in optimal condition for visual processing. For example, the choroid provides essential nutrients to the retina, while the aqueous and vitreous humors help maintain the eye’s shape and internal pressure.

The Refractive System: How the Eye Focuses Light

Visual acuity, or the sharpness of vision, depends on the eye’s ability to refract (bend) light accurately. As light passes through the eye, it encounters structures of varying densities, each playing a role in focusing the light onto the retina:

Cornea: Provides about two-thirds of the eye’s refractive power
Aqueous humor: Helps maintain the shape of the cornea
Lens: Provides fine-tuning of focus, especially for near objects
Vitreous humor: Maintains the eye’s shape and helps focus light

The lens is the adjustable component of this refractive system. Its shape can be altered by the contraction or relaxation of the ciliary muscle, allowing the eye to focus on objects at various distances. This process is known as accommodation.

The Mechanism of Accommodation

How does the eye adjust its focus for objects at different distances? The process of accommodation involves the following steps:

When viewing a distant object, the ciliary muscle relaxes, causing the lens to flatten
For near objects, the ciliary muscle contracts, allowing the lens to become more convex
This change in lens shape alters its refractive power, focusing light from near or far objects onto the retina

The ability to accommodate decreases with age, leading to presbyopia, a condition where near vision becomes increasingly difficult.

The Retina: The Eye’s Light-Sensitive Layer

The retina is the crucial component of the eye where light is converted into electrical signals. This thin layer of tissue at the back of the eye contains two types of photoreceptor cells: rods and cones. Each type has specific characteristics and functions:

Rod Cells: Specialists in Low-Light Vision

Rod cells are primarily responsible for scotopic vision, or vision in low-light conditions. Key features of rod cells include:

High abundance: Approximately 90 million rod cells in the human retina
Maximum density: 15 to 20 degrees from the fovea
High sensitivity: Can detect even a single photon of light
Achromatic vision: Do not contribute to color perception

Cone Cells: Color Vision and High Acuity

Cone cells are active in brighter light conditions and provide color vision and high spatial acuity. Important characteristics of cone cells include:

Lower abundance: Approximately 6 million cone cells in the human retina
Highest density in the fovea: A small depression in the retina where visual acuity is highest
Three types: S-cones (short wavelength), M-cones (medium wavelength), and L-cones (long wavelength)
Faster response time compared to rods

The distribution and characteristics of rods and cones in the retina contribute to the varying capabilities of human vision across different lighting conditions and visual tasks.

The Biochemistry of Vision: How Photoreceptors Detect Light

The process of converting light into electrical signals in photoreceptor cells involves a complex series of biochemical reactions. At the heart of this process are photopigment molecules embedded in the membranes of the photoreceptors. Let’s explore the mechanism in rod cells, which use the photopigment rhodopsin:

The Structure and Function of Rhodopsin

Rhodopsin is a G-protein-coupled receptor composed of two main components:

Scotopsin: A protein with seven transmembrane domains
Retinal: A vitamin A derivative that serves as the light-sensitive component

The process of light detection and signal transduction in rod cells involves the following steps:

Light absorption: A photon is absorbed by the retinal molecule, causing it to change from 11-cis-retinal to all-trans-retinal
Conformational changes: This isomerization leads to a series of shape changes in the rhodopsin molecule
G-protein activation: The activated rhodopsin (Meta II) triggers the G protein transducin
Enzyme cascade: Transducin activates cGMP phosphodiesterase, leading to the breakdown of cGMP
Channel closure: The reduction in cGMP causes cGMP-dependent cation channels to close
Hyperpolarization: The rod cell hyperpolarizes, altering its release of neurotransmitters

This cascade of events ultimately leads to the generation of electrical signals that can be transmitted to the brain via the optic nerve.

The Cone Pigment System

While the basic mechanism is similar in cone cells, they utilize different photopigments:

S-cones: Contain a pigment sensitive to short wavelengths (blue light)
M-cones: Contain a pigment sensitive to medium wavelengths (green light)
L-cones: Contain a pigment sensitive to long wavelengths (red light)

The genes for these cone pigments are located on different chromosomes, with the S-cone gene on chromosome 7 and the M-cone and L-cone genes on the X chromosome.

Adaptation: How the Eye Adjusts to Changing Light Conditions

The human eye has a remarkable ability to function across a wide range of light intensities, from bright sunlight to near darkness. This capability is due to various adaptation mechanisms:

Pupillary Light Reflex

The pupillary light reflex is a rapid response to changes in light intensity:

In bright light: The pupil constricts, reducing the amount of light entering the eye
In dim light: The pupil dilates, allowing more light to reach the retina

This reflex is controlled by the autonomic nervous system and occurs within seconds.

Photochemical Adaptation

Photochemical adaptation involves changes in the sensitivity of photoreceptors:

Dark adaptation: As the eye adjusts to darkness, rhodopsin levels in rods increase, enhancing sensitivity to light
Light adaptation: In bright conditions, photopigments are bleached, reducing sensitivity to prevent overstimulation

This process can take several minutes to complete fully.

Neural Adaptation

Neural adaptation occurs at various levels of the visual system:

Retinal level: Horizontal and amacrine cells in the retina adjust the sensitivity of photoreceptors and ganglion cells
Brain level: Higher visual processing centers in the brain adapt to overall light levels and contrast

These adaptation mechanisms allow the visual system to maintain optimal sensitivity and performance across varying light conditions.

Visual Processing: From Retina to Brain

The journey of visual information doesn’t end at the retina. The signals generated by photoreceptors undergo significant processing before reaching the brain:

Retinal Processing

Within the retina, several layers of neurons process visual information:

Bipolar cells: Receive input from photoreceptors and transmit signals to ganglion cells
Horizontal cells: Provide lateral interactions between photoreceptors, enhancing contrast
Amacrine cells: Modulate the output of bipolar cells and provide input to ganglion cells
Ganglion cells: Integrate information and send action potentials along the optic nerve

This retinal processing begins the extraction of important visual features such as edges, motion, and color contrasts.

The Visual Pathway to the Brain

Visual information travels from the retina to the brain via the following path:

Optic nerve: Carries signals from the retina
Optic chiasm: Where some fibers from each eye cross to the opposite side of the brain
Optic tract: Carries signals to the lateral geniculate nucleus (LGN) of the thalamus
LGN: Relays information to the primary visual cortex
Primary visual cortex: The first stage of cortical processing, located in the occipital lobe

From the primary visual cortex, information is distributed to various higher-order visual areas for more complex processing of features like color, motion, and object recognition.

Common Visual Disorders and Their Physiological Basis

Understanding the physiology of the eye provides insights into various visual disorders:

Refractive Errors

Refractive errors occur when the eye cannot focus light properly on the retina:

Myopia (nearsightedness): The eye focuses light in front of the retina
Hyperopia (farsightedness): The eye focuses light behind the retina
Astigmatism: Irregular curvature of the cornea or lens causes distorted vision

These conditions result from variations in the shape of the eye or its refractive components.

Age-Related Conditions

Several eye conditions become more common with age:

Presbyopia: Loss of accommodation ability, making it difficult to focus on near objects
Cataracts: Clouding of the lens, leading to decreased visual acuity
Age-related macular degeneration: Deterioration of the macula, affecting central vision

These conditions often result from cumulative damage or natural aging processes in ocular tissues.

Retinal Disorders

Disorders affecting the retina can have significant impacts on vision:

Retinitis pigmentosa: A genetic disorder causing progressive loss of rod and cone cells
Diabetic retinopathy: Damage to retinal blood vessels due to diabetes
Retinal detachment: Separation of the retina from the underlying tissue, potentially leading to vision loss

Understanding the physiological basis of these disorders is crucial for developing effective treatments and preventive strategies.

The intricate physiology of the eye enables the remarkable feat of vision, allowing us to perceive and interact with the world around us. From the initial capture of light by the cornea to the complex processing in the retina and brain, each component plays a vital role in creating our visual experience. Ongoing research in ocular physiology continues to deepen our understanding of this fascinating sensory system, paving the way for advancements in eye care and treatment of visual disorders.

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

1.: 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]
2.: 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]
3.: 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]
4.: Lamb TD, Hunt DM. Evolution of the vertebrate phototransduction cascade activation steps. Dev Biol. 2017 Nov 01;431(1):77-92. [PubMed: 28347645]
5.: 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]
6.: Chen CK. RGS Protein Regulation of Phototransduction. Prog Mol Biol Transl Sci. 2015;133:31-45. [PMC free article: PMC4664578] [PubMed: 26123301]
7.: 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]
8.: 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]
9.: 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]
10.: 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]
11.: 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]
12.: 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]
13.: Mehta S. Age-Related Macular Degeneration. Prim Care. 2015 Sep;42(3):377-91. [PubMed: 26319344]
14.: 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]
15.: Pershing S, Pal Chee C, Asch SM, Baker LC, Boothroyd D, Wagner TH, Bundorf MK. Treating age-related macular degeneration: comparing the use of two drugs among medicare and veterans affairs populations. Health Aff (Millwood). 2015 Feb;34(2):229-38. [PubMed: 25646102]
16.: Chiras D, Kitsos G, Petersen MB, Skalidakis I, Kroupis C. Oxidative stress in dry age-related macular degeneration and exfoliation syndrome. Crit Rev Clin Lab Sci. 2015 Feb;52(1):12-27. [PubMed: 25319011]
17.: van Lookeren Campagne M, LeCouter J, Yaspan BL, Ye W. Mechanisms of age-related macular degeneration and therapeutic opportunities. J Pathol. 2014 Jan;232(2):151-64. [PubMed: 24105633]
18.: Zhang K, Zhang L, Weinreb RN. Ophthalmic drug discovery: novel targets and mechanisms for retinal diseases and glaucoma. Nat Rev Drug Discov. 2012 Jun 15;11(7):541-59. [PubMed: 22699774]
19.: 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]
20.: Sasongko MB, Wong TY, Jenkins AJ, Nguyen TT, Shaw JE, Wang JJ. Circulating markers of inflammation and endothelial function, and their relationship to diabetic retinopathy. Diabet Med. 2015 May;32(5):686-91. [PubMed: 25407692]
21.: Frank RN. Diabetic retinopathy and systemic factors. Middle East Afr J Ophthalmol. 2015 Apr-Jun;22(2):151-6. [PMC free article: PMC4411610] [PubMed: 25949071]
22.: He Y, Zhang Y, Su G. Recent advances in treatment of retinitis pigmentosa. Curr Stem Cell Res Ther. 2015;10(3):258-65. [PubMed: 25345673]
23.: He Y, Zhang Y, Liu X, Ghazaryan E, Li Y, Xie J, Su G. Recent advances of stem cell therapy for retinitis pigmentosa. Int J Mol Sci. 2014 Aug 20;15(8):14456-74. [PMC free article: PMC4159862] [PubMed: 25141102]
24.: Natarajan S. Decoding retinitis pigmentosa. Indian J Ophthalmol. 2013 Mar;61(3):91-4. [PMC free article: PMC3665053] [PubMed: 23514641]

: 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.