Eyes physiology. The Intricate Physiology of the Human Eye: From Light Reception to Visual Processing

28.11.202010.07.2023 by alexxlab

How does the human eye function to process light and create visual perception. What are the key structures involved in focusing light onto the retina. How do photoreceptor cells in the retina convert light into electrical signals. What is the difference between rod and cone cells in the retina. How does the brain interpret signals from the optic nerve to form images.

Содержание

The Fundamental Structures of the Eye and Their Functions

The human eye is a marvel of biological engineering, capable of receiving and processing light to create our visual perception of the world. To understand its physiology, we must first examine its key structures:

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
Pupil: The dark center of the iris that allows light to pass through
Lens: The transparent structure behind the iris that focuses light rays
Retina: The light-sensitive layer at the back of the eye
Optic nerve: The nerve that carries visual information from the retina to the brain

Each of these components plays a crucial role in the visual process. But how do they work together to create vision?

The Light’s Journey Through the Eye

When light enters the eye, it first passes through the cornea, which begins the process of focusing the light. The light then travels through the aqueous humor, a clear fluid in the front part of the eye, before reaching the pupil. The iris controls the size of the pupil, adjusting how much light enters the eye.

After passing through the pupil, the light reaches the lens. The lens further focuses the light, adjusting its shape to accommodate for viewing objects at different distances. This process, known as accommodation, is controlled by the ciliary muscles.

Finally, the focused light passes through the vitreous humor, a gel-like substance filling the back of the eye, before reaching the retina. But what happens when the light hits the retina?

The Retina: Where Light Becomes Electrical Signals

The retina is a complex layer of neural tissue lining the back of the eye. It contains two types of photoreceptor cells: rods and cones. These cells are responsible for converting light into electrical signals that can be interpreted by the brain.

Rods: Masters of Low-Light Vision

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

Scotopic vision (vision in low light conditions)
Peripheral vision
Detection of motion

Rods are incredibly sensitive and can detect even a single photon of light. However, they do not provide color vision and have lower spatial resolution compared to cones.

Cones: Color Vision and High Acuity

Cones, on the other hand, are less numerous, with about 6 million in each human retina. They are responsible for:

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

There are three types of cones, each sensitive to different wavelengths of light: S-cones (short wavelength), M-cones (medium wavelength), and L-cones (long wavelength). This trichromatic system allows us to perceive a wide range of colors.

The Molecular Mechanism of Phototransduction

How exactly do photoreceptor cells convert light into electrical signals? This process, known as phototransduction, is a complex cascade of molecular events.

Rhodopsin: The Light-Sensitive Protein

In rod cells, the key player in this process is a protein called rhodopsin. Rhodopsin consists of two parts:

Scotopsin: A protein that forms the structure of rhodopsin
Retinal: A vitamin A derivative that acts as the light-sensitive component

When a photon of light hits rhodopsin, it causes a conformational change in the retinal molecule. This change triggers a cascade of events that ultimately leads to the hyperpolarization of the rod cell and the release of neurotransmitters.

The Phototransduction Cascade

The phototransduction cascade involves several steps:

Light causes retinal to change from 11-cis-retinal to all-trans-retinal
This change activates the G protein transducin
Activated transducin stimulates cGMP phosphodiesterase
cGMP phosphodiesterase breaks down cGMP
Reduced cGMP levels cause cGMP-dependent ion channels to close
The closure of these channels leads to hyperpolarization of the rod cell

This process is remarkably sensitive and efficient, allowing our eyes to detect even very low levels of light.

Visual Acuity and Refraction

Visual acuity, or the sharpness of vision, depends on the proper refraction of light as it passes through the eye. But what factors influence refraction in the eye?

The Refractive Components of the Eye

Several structures in the eye contribute to refraction:

Cornea: Provides about two-thirds of the eye’s refractive power
Aqueous humor: Helps maintain the shape of the cornea
Lens: Provides the remaining one-third of refractive power and allows for accommodation
Vitreous humor: Helps maintain the shape of the eye

The ability to focus on objects at different distances is crucial for clear vision. How does the eye achieve this?

Accommodation: Focusing Near and Far

Accommodation is the process by which the eye changes optical power to maintain a clear image of an object as its distance varies. This is primarily achieved through changes in the shape of the lens:

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

This ability to adjust focus allows us to maintain clear vision across a range of distances.

The Visual Pathway: From Retina to Brain

Once photoreceptors have converted light into electrical signals, how does this information reach the brain? The visual pathway is a complex network of neurons that carries visual information from the eye to the visual cortex of the brain.

The Optic Nerve and Beyond

The journey of visual information 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 nerves from both eyes meet at the optic chiasm
Visual information continues through the optic tract to the lateral geniculate nucleus
From there, signals are sent to the primary visual cortex in the occipital lobe

This pathway ensures that visual information from both eyes is integrated and processed to form a cohesive visual perception.

Color Vision: The Trichromatic Theory

The ability to perceive color adds richness and depth to our visual experience. But how does color vision work?

The Three Types of Cone Cells

Color vision in humans is based on the presence of 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 combination of signals from these three types of cones allows us to perceive a wide spectrum of colors. This is known as the trichromatic theory of color vision.

Color Processing in the Brain

The perception of color isn’t just about the initial detection of wavelengths by cone cells. The brain plays a crucial role in processing and interpreting color information:

Opponent process theory: Explains how the brain processes contrasting color pairs
Color constancy: The ability to perceive colors consistently under different lighting conditions
Color memory: The brain’s ability to remember and recognize colors

These processes work together to create our rich perception of color in the world around us.

Maintaining Eye Health: Supportive Structures and Systems

While the process of vision is fascinating, it’s equally important to understand the structures and systems that maintain eye health and function.

The Choroid: Nourishing the Eye

The choroid is a layer of blood vessels between the retina and the sclera (the white of the eye). It plays several crucial roles:

Provides oxygen and nutrients to the outer layers of the retina
Helps regulate eye temperature
Absorbs light to prevent internal reflection within the eye

Without the choroid, the retina would not be able to function properly.

The Lacrimal System: More Than Just Tears

The lacrimal system, responsible for tear production and drainage, is essential for eye health:

Keeps the cornea moist and nourished
Washes away debris and foreign particles
Contains antimicrobial compounds to protect against infection
Provides a smooth optical surface for clear vision

Proper function of the lacrimal system is crucial for maintaining clear vision and eye comfort.

Intraocular Pressure: A Delicate Balance

Maintaining the correct pressure within the eye is vital for its proper function. This intraocular pressure (IOP) is regulated by the production and drainage of aqueous humor:

Produced by the ciliary body
Flows through the pupil into the anterior chamber
Drains through the trabecular meshwork and Schlemm’s canal

Imbalances in IOP can lead to conditions such as glaucoma, highlighting the importance of this often-overlooked aspect of eye physiology.

The physiology of the eye is a testament to the incredible complexity and efficiency of biological systems. From the initial capture of light to the final perception of a visual image, each step involves intricate processes and specialized structures. Understanding these processes not only satisfies our curiosity about how we see the world but also provides crucial insights for maintaining eye health and treating visual disorders. As research continues, we may uncover even more fascinating aspects of eye physiology, potentially leading to new treatments and technologies to enhance and protect our vision.

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.