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

27.11.202010.07.2023 by alexxlab

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

Содержание

The Fundamental Structures of the Human Eye

The human eye is a marvel of biological engineering, designed to capture and process light to create our visual perception of the world. Its proper function relies on several key structures working in harmony:

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
Choroid: A layer of blood vessels that nourishes the retina
Aqueous and vitreous humor: Fluids that maintain the eye’s shape and pressure
Lacrimal system: Produces tears to keep the eye moist and protected

Each of these components plays a crucial role in the process of vision. The cornea and lens work together to refract light, focusing it precisely onto the retina. The iris adjusts to control the amount of light entering the eye, while the ciliary body fine-tunes the shape of the lens for optimal focus. The retina, with its specialized cells, converts light into electrical signals that are then transmitted to the brain via the optic nerve.

The Retina: Where Light Becomes Sight

The retina is the powerhouse of visual processing in the eye. It contains two primary types of photoreceptor cells: rods and cones. These cells are responsible for converting light into electrical signals that the brain can interpret as visual information.

Rods: Masters of Low-Light Vision

Rods are the more numerous of the two photoreceptor types, with approximately 90 million present in the human retina. They are primarily responsible for:

Scotopic vision (vision in low-light conditions)
Peripheral vision
Motion detection

Rods are incredibly sensitive to light, capable of detecting even a single photon. They reach their maximum density about 15 to 20 degrees from the fovea, a small depression in the retina where visual acuity is highest.

Cones: Providers of Color and Detail

While less numerous than rods (approximately 6 million in the human retina), cones are essential for:

Color vision
High visual acuity
Photopic vision (vision in well-lit conditions)

Cones are concentrated in the fovea, which is responsible for our sharp, central vision. There are three types of cones, each sensitive to different wavelengths of light: S-cones (short), M-cones (medium), and L-cones (long). This trichromatic system allows us to perceive a wide range of colors.

The Biochemistry of Vision: From Light to Neural Signals

The process of converting light into neural signals is a complex biochemical cascade that begins in the photoreceptor cells. This process, known as phototransduction, involves several key steps:

Light absorption by photopigments
Conformational changes in the photopigment molecule
Activation of G-proteins
Activation of enzymes that alter ion channel activity
Changes in cell membrane potential
Neurotransmitter release

Rhodopsin: The Light-Sensitive Protein in Rods

In rod cells, the primary photopigment is rhodopsin. This G-protein-coupled receptor consists of two main components:

Scotopsin: The protein component
Retinal: A vitamin A derivative that acts as the light-sensitive cofactor

When light strikes rhodopsin, it triggers a series of conformational changes that ultimately lead to the hyperpolarization of the rod cell and the release of neurotransmitters.

The Phototransduction Cascade: A Molecular Symphony

The phototransduction cascade is a remarkable example of molecular signaling in biology. Here’s a step-by-step breakdown of the process in rod cells:

Light causes 11-cis-retinal to isomerize to all-trans-retinal
This change activates the rhodopsin molecule, forming metarhodopsin II
Metarhodopsin II activates the G-protein transducin
The alpha subunit of transducin, bound to GTP, activates cGMP phosphodiesterase
cGMP phosphodiesterase hydrolyzes cGMP, reducing its concentration
The reduction in cGMP causes cGMP-dependent cation channels to close
This leads to hyperpolarization of the rod cell
Hyperpolarization results in a decrease in glutamate release

This cascade amplifies the signal from a single photon, allowing rods to detect even the faintest light. The process in cones is similar but involves different photopigments and has a lower amplification factor, contributing to their reduced light sensitivity but increased temporal resolution.

Adaptation and Recovery: The Eye’s Dynamic Response

The human eye must constantly adapt to changing light conditions. This process, known as light adaptation, involves several mechanisms:

Pupillary light reflex: The iris constricts or dilates to control light entry
Photochemical adaptation: Changes in photopigment concentrations
Neural adaptation: Adjustments in neural signaling pathways

Recovery from light exposure is equally important. In rod cells, this involves:

Rhodopsin kinase phosphorylating the cytosolic tail of rhodopsin
Arrestin binding to phosphorylated rhodopsin to further inactivate it
RGS proteins increasing the rate of GTP to GDP hydrolysis in transducin
Restoration of cGMP levels through activation of guanylyl cyclase

These processes allow the eye to maintain sensitivity across a wide range of light intensities and to quickly recover from bright light exposure.

Visual Acuity and Refraction: Focusing on Detail

Visual acuity, or the ability to see fine detail, depends on proper refraction of light through the eye’s structures. The cornea provides about two-thirds of the eye’s refractive power, while the lens provides the remaining third and allows for dynamic focusing through a process called accommodation.

The Role of the Lens in Accommodation

Accommodation is the process by which the eye changes optical power to maintain focus on objects at varying distances. This is achieved through the action of the ciliary muscles:

For near objects: Ciliary muscles contract, allowing the lens to become more convex
For distant objects: Ciliary muscles relax, causing the lens to flatten

This dynamic adjustment allows for clear vision across a range of distances. However, the ability to accommodate decreases with age, leading to presbyopia, a condition where near vision becomes increasingly difficult.

The Neural Pathways of Vision: From Eye to Brain

The visual information captured by the retina must be transmitted to the brain for processing and interpretation. This journey involves several key steps:

Photoreceptors synapse with bipolar cells in the retina
Bipolar cells synapse with ganglion cells
Axons of ganglion cells form the optic nerve
The optic nerve exits the eye at the optic disc (creating the “blind spot”)
Optic nerves from both eyes partially cross at the optic chiasm
Visual information is relayed to the lateral geniculate nucleus of the thalamus
From the thalamus, signals are sent to the primary visual cortex in the occipital lobe

This complex pathway allows for the integration of visual information from both eyes and the processing of different aspects of visual stimuli, such as motion, color, and form.

Common Visual Disorders and Their Physiological Basis

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

Myopia (nearsightedness): Typically caused by an elongated eyeball or overly curved cornea
Hyperopia (farsightedness): Often due to a shortened eyeball or flattened cornea
Astigmatism: Results from an irregularly shaped cornea
Glaucoma: Increased intraocular pressure damaging the optic nerve
Cataracts: Clouding of the lens, often age-related
Macular degeneration: Deterioration of the central portion of the retina
Color blindness: Typically due to genetic defects in cone photopigments

Each of these conditions can be traced back to specific physiological or structural abnormalities in the eye, highlighting the importance of understanding ocular physiology in diagnosing and treating visual disorders.

Emerging Research and Future Directions in Eye Physiology

The field of eye physiology continues to evolve, with ongoing research in several exciting areas:

Gene therapy for inherited retinal diseases
Stem cell treatments for retinal regeneration
Advanced retinal prosthetics for restoring vision
Optogenetics for manipulating neural activity in the visual system
Artificial intelligence in diagnosing and monitoring eye diseases
Development of novel drug delivery systems for ocular treatments

These areas of research hold promise for developing new treatments for previously incurable eye conditions and enhancing our understanding of visual processing.

As our knowledge of eye physiology continues to expand, so too does our ability to maintain and restore vision. From the intricate biochemical cascades within photoreceptor cells to the complex neural networks that process visual information, the study of eye physiology remains a fascinating and vital field of research. By unraveling the mysteries of how we see, scientists and clinicians are paving the way for innovative therapies and technologies that could revolutionize eye care and potentially restore sight to those affected by visual impairments.

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.