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

28.11.202010.07.2023 by alexxlab

How does the eye function to process light and create vision. What are the key structures involved in eye physiology. How do rods and cones in the retina enable visual perception. What is the mechanism of phototransduction in the human eye.

Содержание

The Fundamental Structures of the Human Eye

The human eye is a marvel of biological engineering, comprising several intricate structures that work in harmony to enable vision. At its core, the eye’s primary function is to receive light from the environment and convert it into electrical signals that the brain can interpret. But how exactly does this process unfold?

The key structures involved in eye physiology include:

Cornea: The transparent front layer that initially refracts light
Iris: The colored portion that controls the amount of light entering the eye
Pupil: The adjustable opening at the center of the iris
Lens: The flexible structure that further focuses light onto the retina
Retina: The light-sensitive layer at the back of the eye containing photoreceptors
Optic nerve: The pathway that transmits visual information to the brain

Each of these components plays a crucial role in the visual process. The cornea and lens work together to focus light onto the retina, while the iris adjusts the pupil size to control light intensity. But it’s the retina that truly stands out as the powerhouse of visual perception.

The Retina: Where Light Becomes Sight

The retina is a complex neural tissue lining the back of the eye. It’s here that the magic of phototransduction occurs – the process by which light energy is converted into electrical signals. But what makes the retina so special?

The retina contains two types of photoreceptor cells:

Rods: Specialized for low-light vision (scotopic vision)
Cones: Responsible for color vision and high visual acuity

Rods are incredibly numerous, with approximately 90 million present in the human retina. They’re most densely packed about 15 to 20 degrees from the fovea, a small depression in the retina where visual acuity is highest. Rods are exquisitely sensitive to light, allowing us to see in dim conditions, but they don’t provide color information.

Cones, on the other hand, are less numerous (about 6 million in the human retina) but are responsible for our color vision and high visual acuity. They’re concentrated in the fovea, which is actually free of rods. This arrangement allows for the sharpest vision to be in the center of our visual field.

The Unique Properties of Rods and Cones

How do rods and cones differ in their function? Rods have more photopigment and exhibit high amplification, which contributes to their superior light sensitivity. They also have highly convergent retinal pathways, meaning multiple rod cells can feed into a single nerve fiber, further enhancing sensitivity at the cost of visual acuity.

Cones, in contrast, have a faster response time and shorter integration times. They’re also directionally selective, meaning they respond differently to light coming from different angles. This property, combined with their concentration in the fovea, contributes to the high visual acuity we experience in the center of our visual field.

The Molecular Basis of Vision: Photopigments and Phototransduction

At the molecular level, vision begins with photopigments – light-sensitive molecules embedded in the membranes of photoreceptors. But what exactly are these photopigments, and how do they work?

In rods, the photopigment is called rhodopsin. It’s a complex molecule consisting of two main parts:

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

Rhodopsin is a G-protein-coupled receptor, a type of protein that’s crucial for many cellular signaling processes. It’s made up of 348 amino acids arranged in seven transmembrane domains, with the gene encoding it located on chromosome 3.

The Phototransduction Cascade

When light strikes rhodopsin, it triggers a fascinating cascade of molecular events. How does this process unfold?

Light causes retinal to change from its inactive 11-cis-retinal form to all-trans-retinal.
This change leads to a series of conformational changes in rhodopsin, resulting in its activated form, metarhodopsin II (Meta II).
Meta II activates a G protein called transducin.
The alpha subunit of transducin, now bound to GTP, activates cGMP phosphodiesterase.
This enzyme hydrolyzes cGMP, leading to the closure of cGMP-dependent cation channels.
The closure of these channels causes the rod cell to hyperpolarize, altering its release of neurotransmitters.

This cascade amplifies the signal tremendously – a single photon can lead to the hydrolysis of more than a million cGMP molecules, allowing rods to detect even very low levels of light.

Color Vision: The Role of Cone Photoreceptors

While rods are crucial for low-light vision, it’s the cones that give us our rich, colorful visual experience. But how exactly do cones enable color vision?

Humans have 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)

This trichromatic arrangement allows our visual system to distinguish between millions of different colors. The genes for these cone photopigments are located on different chromosomes – the S-cone gene is on chromosome 7, while the M-cone and L-cone genes are on the X chromosome.

The distribution of these cone types in the retina is not uniform. The fovea, which provides our sharpest vision, contains mostly L-cones and M-cones, with S-cones largely absent from this region. This arrangement contributes to our high visual acuity for red and green colors compared to blue.

The Cone Mosaic

In the fovea, cones are arranged in a specific pattern known as the “cone mosaic.” This arrangement optimizes color perception and visual acuity. The mosaic consists of a regular pattern of L-cones and M-cones, with occasional S-cones interspersed.

The ratio of L-cones to M-cones varies among individuals but is typically around 2:1. This variation can lead to subtle differences in color perception between individuals, although most people with normal color vision can distinguish the same range of colors.

Adaptation: How the Eye Adjusts to Changing Light Conditions

Our visual system has an impressive ability to function across a wide range of light intensities, from starlight to bright sunlight. But how does the eye manage this feat?

The process of adaptation involves several mechanisms:

Pupillary light reflex: The iris constricts or dilates to control the amount of light entering the eye.
Photochemical adaptation: The photopigments in rods and cones adjust their sensitivity.
Neural adaptation: The visual processing system adjusts its sensitivity.

Dark adaptation occurs when we move from a bright environment to a dark one. Initially, cone sensitivity increases rapidly, but after about 10 minutes, rod sensitivity begins to increase dramatically. Full dark adaptation can take up to 30 minutes.

Light adaptation, on the other hand, occurs much more quickly. When we move from darkness to light, our pupils constrict rapidly, and our photoreceptors quickly adjust their sensitivity to prevent oversaturation.

The Role of Photopigment Regeneration

A crucial part of adaptation is the regeneration of photopigments. When light activates a photopigment, it becomes “bleached” and must be regenerated before it can respond to light again. This process, known as the visual cycle, involves a series of enzymatic reactions that convert all-trans-retinal back to 11-cis-retinal.

In rods, this regeneration process occurs in the retinal pigment epithelium (RPE), a layer of cells just outside the retina. Cones, however, have an additional mechanism that allows for faster pigment regeneration, contributing to their ability to function well in bright light conditions.

Visual Processing: From Retina to Brain

While the retina is where vision begins, it’s in the brain where visual information is processed and interpreted. But how does visual information travel from the eye to the brain?

The pathway from eye to brain involves several steps:

Photoreceptors (rods and cones) detect light and initiate the visual signal.
This signal is passed to bipolar cells, which in turn activate ganglion cells.
The axons of ganglion cells form the optic nerve, which carries visual information out of the eye.
The optic nerves from both eyes partially cross at the optic chiasm.
Visual information then travels through the optic tract to the lateral geniculate nucleus (LGN) of the thalamus.
From the LGN, signals are sent to the primary visual cortex in the occipital lobe of the brain.

This pathway preserves the spatial organization of the visual field, creating a retinotopic map in the visual cortex. This means that neighboring areas in the visual field are represented by neighboring areas in the cortex.

Parallel Processing in the Visual System

The visual system doesn’t just process a single stream of information. Instead, different aspects of the visual scene are processed in parallel. There are two main pathways:

The parvocellular pathway: Processes fine detail and color information
The magnocellular pathway: Processes information about motion and depth

These pathways begin in the retina and remain largely separate through the LGN and into the visual cortex. This parallel processing allows for efficient analysis of different aspects of the visual scene.

Eye Movements: Stabilizing and Directing Gaze

Our eyes are constantly in motion, even when we think we’re fixating on a single point. These movements are crucial for maintaining clear and stable vision. But what types of eye movements are there, and how do they contribute to our visual experience?

There are several types of eye movements:

Saccades: Rapid, ballistic movements that quickly change the point of fixation
Smooth pursuit: Slower tracking movements that allow the eyes to follow a moving target
Vergence: Movements that allow both eyes to focus on the same point in space
Vestibulo-ocular reflex: Movements that stabilize the eyes when the head moves
Optokinetic reflex: Movements that stabilize the image on the retina during sustained motion

These movements are controlled by six extraocular muscles attached to each eye. The coordinated action of these muscles allows for precise control of eye position and movement.

The Role of Eye Movements in Visual Perception

Eye movements play a crucial role in visual perception. Saccades, for example, allow us to rapidly shift our gaze to different parts of a scene, building up a detailed mental image. Smooth pursuit movements enable us to track moving objects, crucial for tasks like driving or watching sports.

Interestingly, during saccades, visual perception is suppressed. This saccadic suppression prevents us from perceiving the rapid motion blur that would otherwise occur. Our brain fills in this gap, creating the illusion of continuous, stable vision.

The vestibulo-ocular reflex and optokinetic reflex work together to stabilize our vision during head and body movements. Without these reflexes, our visual world would appear to bounce and shift with every step we take.

The Aging Eye: Changes in Visual Function Over Time

As we age, our eyes undergo various changes that can affect our vision. Understanding these changes is crucial for maintaining eye health and adapting to the visual challenges of aging. But what exactly happens to our eyes as we get older?

Several age-related changes occur in the eye:

Presbyopia: Decreased ability to focus on near objects due to lens hardening
Decreased pupil size: Reduces the amount of light entering the eye
Decreased color perception: Particularly for blue hues
Increased susceptibility to glare
Decreased tear production: Can lead to dry eye syndrome
Increased risk of eye diseases: Such as cataracts, glaucoma, and age-related macular degeneration

Presbyopia typically begins to develop around age 40 and progresses until about age 65. It’s caused by a gradual loss of flexibility in the lens, making it harder to focus on close objects. This is why many people start needing reading glasses in their 40s.

Adaptations and Interventions for Age-Related Vision Changes

While some age-related vision changes are inevitable, there are various ways to adapt to these changes and maintain good visual function:

Regular eye exams: Early detection of eye problems can lead to more effective treatment
Proper lighting: Increased illumination can compensate for decreased light sensitivity
Corrective lenses: Glasses or contact lenses can address refractive errors and presbyopia
Lifestyle changes: A healthy diet and exercise can promote overall eye health
Protective measures: Sunglasses and avoiding smoking can protect against some age-related eye changes

Additionally, advances in medical technology offer new interventions for age-related eye conditions. For example, multifocal intraocular lenses can be implanted during cataract surgery to address both distance and near vision needs.

Understanding the physiology of the eye not only helps us appreciate the complexity of our visual system but also guides the development of strategies to maintain and enhance our vision throughout our lives. As research in this field continues, we can look forward to even better ways to protect and optimize our precious sense of sight.

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.