Retina of the eye: structure and functions, main pathologies. Diagnosis of the body on the retina of the eye Central chorioretinal dystrophy of the retina

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Diagnosis of the body on the retina of the eye - do not miss your disease

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How I want to be a sorceress - look into the eyes and ... make a diagnosis! But there are certain signs that appear in the eyes, under the eyes, which will just say about the developing disease. Yes, and by the dashes on the iris, one or another diagnosis can be suspected.

Of course, this is not a 100% diagnosis, but it is better to be warned and take preventive measures in time, to improve your health, than to remember the roasted rooster again and again.

How many times have we heard in our lives: "Take care of your health from a young age ..."

Did you take care?

Here, that's it! And when it’s not so easy to get up in the morning, there are vague migrating pains in the body, general malaise ... In general, in simple terms: “it hurts paws, ears and tail”, and why it’s not clear!

In this case, you can conduct a small diagnosis of the eyes at home. Of course, this will not be the ultimate truth, but in which medical direction of the disease to look, you decide.

How to determine the disease by the eyes, make a diagnosis

Exist 19 main signs of incipient diseases that can be easily "read" in the eyes.

1. Swelling of the eyes (bags under the eyes) in the morning speaks of diseases of the kidneys, heart.

2. Swelling and redness of the eyelids allows you to think about the manifestation of an allergy (of course, if you do not take into account the banal infectious conjunctivitis, which you can determine by the absence of itching and purulent discharge from the eyes)

3. Involuntary twitching of the eyelids signal neuroticism, and the associated lack of magnesium in the body.

4. Bags under the eyes indicate chronic fatigue, stress.

5. The appearance of red streaks on the sclera (strings of blood vessels) indicates hypertension.

6. Dark circles under the eyes - overwork, chronic fatigue, stress. If the color turns brown or purple, it is worth checking the kidneys, blood sugar, thyroid gland and cardiovascular system.

7. Blueness of proteins - lack of hemoglobin, developing anemia.

8. Yellowness of proteins - first of all, you should think about hepatitis A. Then about other diseases of the liver of the biliary tract.

9. Increased tearing may indicate a cold (if there are additional symptoms of acute respiratory infections), it may indicate an allergy, especially seasonal to plant pollen. Watery eyes for no reason (for example, a strong wind on the street), along with a red drawing of the corneal vessels, will force the ophthalmologist to check if you have glaucoma.

10. Protrusion of the eyeballs makes it possible to suspect the development of hyperthyroidism (increased levels of thyroid hormones), but it is also worth checking with an optometrist for the development of glaucoma.

11. Visual impairment at dusk (night blindness) indicates a lack of vitamin A.

12. Darkening of the edges of the eyes - allows you to suspect a metabolic disorder.

13. Flashes or fiery circles before the eyes occur when cerebral circulation is disturbed, frequent migraines.

14. Swollen upper eyelids may indicate an emerging process of stone formation in the gallbladder.

15. Small dark spots under the eyes will make it possible to suspect the same process, but only in the kidneys.

16. The frequent appearance of barley in front of your eyes will tell not only about the banal infection with dirty hands (most often), but there is another option that there are problems with the liver and gallbladder.

17. The light, almost white color of the inner surface of the eyelid will report a lack of blood circulation (most likely there will be a low level of hemoglobin in the blood), a disorder of the digestive tract or problems in the urogenital area.

18. A shade to red-orange on the same inner surface of the eyelids will tell you that there may be problems with the pancreas, spleen, liver. (Normally it should be a light pink shade).

19. If a whitish mucous coating regularly appears in the eyes, making it difficult to see, it is worth checking for developing cataracts.

Iridology - iris diagnosis

Iridology can also tell about diseases and all kinds of disorders in the functioning of the body.

Iridology - diagnostics on dashes, lines, specks that appear with age on the iris. This science appeared in the 19th century, now, thanks to the accuracy of instruments, it is becoming more and more perfect.

Yes, you yourself can see a very impressive table of correspondence of target organs to places of appearance of dots and dashes on the iris of the eyes:

Thanks

The site provides reference information for informational purposes only. Diagnosis and treatment of diseases should be carried out under the supervision of a specialist. All drugs have contraindications. Expert advice is required!

Depending on which area of ​​the retina has been affected, they are divided into three large groups:
1. Generalized retinal dystrophy;
2. Central retinal dystrophies;
3. Peripheral dystrophies of the retina.

With central dystrophy, only the central part of the entire retina is affected. Since this central part of the retina is called macula, then the term is often used to denote dystrophy of the corresponding localization macular. Therefore, synonymous with the term "central retinal dystrophy" is the concept of "macular retinal dystrophy".

With peripheral dystrophy, the edges of the retina are affected, and the central areas remain intact. With generalized retinal dystrophy, all its parts are affected - both central and peripheral. Standing apart is age-related (senile) retinal dystrophy, which develops against the background of senile changes in the structure of microvessels. According to the localization of the lesion, senile retinal dystrophy is central (macular).

Depending on the characteristics of tissue damage and the course of the disease, central, peripheral and generalized retinal dystrophies are divided into numerous varieties, which will be considered separately.

Central retinal dystrophy - classification and brief description of the varieties

• Macular degeneration Stargardt;
• Yellow-spotted fundus (Franceschetti's disease);
• Yolk (vitelliform) macular degeneration of Best;
• Congenital cone retinal dystrophy;
• Colloidal retinal dystrophy Doyna;
• Age-related retinal degeneration (dry or wet macular degeneration);
• Central serous choriopathy.

Central chorioretinal dystrophy of the retina

Due to the presence of effusion under the retina, a characteristic symptom of this dystrophy is a decrease in visual acuity and the appearance of undulating distortions of the image, as if a person is looking through a layer of water.

Macular (age-related) retinal dystrophy

Both forms of macular degeneration of the retina develop in people over 50-60 years old against the background of senile changes in the structure of the walls of microvessels. Against the background of age-related dystrophy, damage occurs to the vessels of the central part of the retina, the so-called macula, which provides high resolution, that is, it allows a person to see and distinguish the smallest details of objects and the environment at close range. However, even with a severe course of age-related dystrophy, complete blindness occurs extremely rarely, since the peripheral parts of the retina of the eye remain intact and allow a person to partially see. Preserved peripheral parts of the retina of the eye allow a person to navigate normally in his usual environment. In the most severe course of age-related retinal dystrophy, a person loses the ability to read and write.

Dry (non-exudative) age-related macular degeneration The retina of the eye is characterized by the accumulation of waste products of cells between the blood vessels and the retina itself. These waste products are not removed in time due to a violation of the structure and functions of the microvessels of the eye. Waste products are chemicals that are deposited in the tissues under the retina and look like small yellow bumps. These yellow bumps are called Druzes.

Dry retinal degeneration accounts for up to 90% of cases of all macular degeneration and is a relatively benign form, since its course is slow, and therefore the decrease in visual acuity is also gradual. Non-exudative macular degeneration usually proceeds in three successive stages:
1. The early stage of dry age-related macular degeneration of the retina is characterized by the presence of small drusen. At this stage, the person still sees well, he is not bothered by any visual impairment;
2. The intermediate stage is characterized by the presence of either one large drusen or several small ones located in the central part of the retina. These drusen reduce the field of view of a person, as a result of which he sometimes sees a spot in front of his eyes. The only symptom at this stage of age-related macular degeneration is the need for bright light to read or write;
3. The pronounced stage is characterized by the appearance of a spot in the field of view, which has a dark color and a large size. This spot does not allow a person to see most of the surrounding picture.

Wet macular degeneration of the retina occurs in 10% of cases and has an unfavorable prognosis, because against its background, firstly, the risk of developing retinal detachment is very high, and secondly, vision loss occurs very quickly. With this form of dystrophy, new blood vessels begin to actively grow under the retina of the eye, which are normally absent. These vessels have a structure that is not characteristic of the eye, and therefore their shell is easily damaged, and fluid and blood begin to sweat through it, accumulating under the retina. This effusion is called exudate. As a result, exudate accumulates under the retina, which presses on it and gradually exfoliates. That is why wet macular degeneration is dangerous retinal detachment.

With wet macular degeneration of the retina, there is a sharp and unexpected decrease in visual acuity. If treatment is not started immediately, then complete blindness may occur against the background of retinal detachment.

Peripheral retinal dystrophy - classification and general characteristics of species

Peripheral retinal dystrophies are often caused by changes in the length of the eye against the background of progressive myopia and poor blood circulation in this area. Against the background of the progression of peripheral dystrophies, the retina becomes thinner, as a result of which the so-called tractions (areas of excessive tension) are formed. These tractions during prolonged existence create the preconditions for tearing the retina, through which the liquid part of the vitreous body seeps under it, lifts it and gradually peels off.

Depending on the degree of danger of retinal detachment, as well as on the type of morphological changes, peripheral dystrophies are divided into the following types:

• Lattice retinal dystrophy;
• retinal degeneration of the "traces of the cochlea" type;
• Hoarfrost degeneration of the retina;
• Cobblestone retinal degeneration;
• Small cystic degeneration of Blessin-Ivanov;
• Pigmentary dystrophy of the retina;
• Children's tapetoretinal amaurosis of Leber;
• X-chromosome juvenile retinoschisis.

Lattice retinal dystrophy

Most often (in 2/3 of cases), lattice retinal dystrophy is detected in men over 20 years of age, which indicates its hereditary nature. Lattice dystrophy affects one or both eyes with approximately the same frequency and then slowly and gradually progresses throughout a person's life.

With lattice dystrophy, white, narrow, wavy stripes are visible in the fundus, forming lattices or rope ladders. These bands are formed by collapsed and hyaline-filled blood vessels. Between the collapsed vessels, areas of thinning of the retina are formed, which have a characteristic appearance of pinkish or red foci. In these areas of the thinned retina, cysts or tears can form, leading to detachment. The vitreous body in the area adjacent to the area of ​​the retina with dystrophic changes is liquefied. And along the edges of the dystrophy area, the vitreous body, on the contrary, is very tightly soldered to the retina. Because of this, there are areas of excessive tension on the retina (traction), which form small gaps that look like valves. It is through these valves that the liquid part of the vitreous body penetrates under the retina and provokes its detachment.

Peripheral dystrophy of the retina of the type "traces of the cochlea"

Hoarfrost retinal dystrophy

Retinal dystrophy "cobblestone"

Small cystic retinal dystrophy of the eye of Blessin - Ivanov

Pigmentary retinal dystrophy

Leber's pediatric tapetoretinal amaurosis

X-chromosomal juvenile retinoschisis

congenital retinal dystrophy

• Pigmentary dystrophy;
• Amaurosis Leber;
• Nyctalopia (lack of night vision);
• Cone dysfunction syndrome, in which color perception is impaired or there is complete color blindness (everything is seen by a person as gray or black and white).

• Stargardt's disease;
• Best's disease;
• Age-related macular degeneration.

• X-chromosomal juvenile retinoschisis;
• Wagner's disease;
• Goldman-Favre disease.

Retinal dystrophy during pregnancy

If a woman had any eye diseases before pregnancy, for example, myopia, hemeralopia and others, then this significantly increases the risk of developing retinal dystrophy during childbearing. Since various eye diseases are widespread in the population, the development of retinal dystrophy in pregnant women is not uncommon. It is because of the risk of dystrophy with subsequent retinal detachment that gynecologists refer pregnant women for a consultation with an ophthalmologist. And for the same reason, women suffering from myopia need permission from an ophthalmologist to give birth naturally. If the ophthalmologist considers the risk of fulminant dystrophy and retinal detachment in childbirth too high, then he will recommend a caesarean section.

Retinal dystrophy - causes

The local causative factors of retinal dystrophy include the following:

• hereditary predisposition;
• Myopia of any degree of severity;
• Inflammatory diseases of the eyes;
• Postponed operations on the eyes.

• Hypertonic disease;
• Diabetes;
• Transferred viral infections;
• Intoxication of any nature (poisoning with poisons, alcohol, tobacco, bacterial toxins, etc.);
• Elevated blood cholesterol levels;
• Deficiency of vitamins and minerals that enter the body with food;
• Chronic diseases (heart, thyroid, etc.);
• Age-related changes in the structure of blood vessels;
• Frequent exposure to direct sunlight on the eyes;
• White skin and blue eyes.

Retinal dystrophy - symptoms and signs

• Decreased visual acuity in one or both eyes (needing bright light to read or write is also a sign of decreased visual acuity)
• Narrowing of the field of view;
• The appearance of cattle (a blur or feeling of a curtain, mist or obstruction before the eyes);
• Distorted, undulating picture before the eyes, as if a person is looking through a layer of water;
• Poor vision in darkness or twilight (nyctalopia);
• Violation of color discrimination (colors are perceived by others that do not correspond to reality, for example, blue is seen as green, etc.);
• Periodic appearance of "flies" or flashes before the eyes;
• Metamorphopsia (wrong perception of everything related to the shape, color and location in space of a real object);
• The inability to correctly distinguish a moving object from a resting one.

In addition to the listed clinical symptoms, retinal dystrophy is characterized by the following signs detected during objective examinations and various tests:
1. Line distortion on Amsler test. This test consists in the fact that a person alternately looks with each eye at a point located in the center of a grid drawn on a piece of paper. First, the paper is placed at arm's length from the eye, and then slowly brought closer. If the lines are distorted, then this is a sign of macular degeneration of the retina (see Figure 1);


Figure 1 - Amsler test. At the top right is a picture that a person with normal vision sees. At the top left and bottom is the image that a person sees with retinal dystrophy.
2. Characteristic changes in the fundus (for example, drusen, cysts, etc.).
3. Decreased electroretinography.

Retinal dystrophy - photo

This photograph shows cobblestone retinal dystrophy.

This photo shows dry age-related macular degeneration of the retina.

Retinal dystrophy - treatment

General principles of therapy for various types of retinal dystrophy

Drug therapy for retinal dystrophy consists in the use of the following groups of drugs:
1. Antiplatelet agents- drugs that reduce blood clots in the vessels (for example, Ticlopidin, Clopidogrel, acetylsalicylic acid). These drugs are taken orally in the form of tablets or administered intravenously;
2. Vasodilators and angioprotectors - drugs that dilate and strengthen blood vessels (for example, No-shpa, Papaverine, Askorutin, Complamin, etc.). Drugs are taken orally or administered intravenously;
3. Lipid-lowering drugs - drugs that lower blood cholesterol levels, for example, Methionine, Simvastatin, Atorvastatin, etc. The drugs are used only in people suffering from atherosclerosis;
4. Vitamin complexes in which there are elements important for the normal functioning of the eyes, for example, Okuvayt-lutein, Blueberry-forte, etc .;
5. B vitamins ;
6. Preparations that improve microcirculation , for example, Pentoxifylline. Usually drugs are injected directly into the structures of the eye;
7. Polypeptides obtained from the retina of cattle (drug Retinolamine). The drug is injected into the structures of the eye;
8. Eye drops containing vitamins and biological substances that promote reparation and improve metabolism, for example, Taufon, Emoksipin, Oftalm-Katahrom, etc .;
9. Lucentis- an agent that prevents the growth of pathological blood vessels. It is used for the treatment of age-related macular degeneration of the retina.

The listed drugs are taken in courses, several times (at least twice) during the year.

In addition, with wet macular degeneration, Dexamethasone is injected into the eye, and Furosemide intravenously. With the development of hemorrhages in the eye, in order to resolve it as soon as possible and stop it, heparin, Etamzilat, aminocaproic acid or Prourokinase are administered intravenously. To relieve swelling in any form of retinal dystrophy, Triamcinolone is injected directly into the eye.

Also, courses for the treatment of retinal dystrophies use the following methods of physiotherapy:

• Electrophoresis with heparin, No-shpa and nicotinic acid;
• Photostimulation of the retina;
• Stimulation of the retina with low-energy laser radiation;
• Electrical stimulation of the retina;
• Intravenous laser blood irradiation (ILBI).

• Laser coagulation of the retina;
• vitrectomy;
• Vasoreconstructive operations (crossing of the superficial temporal artery);
• revascularization operations.

Approaches to the treatment of macular degeneration of the retina

If macular degeneration is in a more severe stage, then along with drug treatment, physiotherapy methods are used, such as:

• Magnetic stimulation of the retina;
• Photostimulation of the retina;
• Laser stimulation of the retina;
• Electrical stimulation of the retina;
• Intravenous laser blood irradiation (ILBI);
• Operations to restore normal blood flow in the retina.

If a person has wet dystrophy, then first of all, laser coagulation of sprouting, abnormal vessels is performed. During this procedure, a laser beam is directed to the affected areas of the retina, and under the influence of its powerful energy, the blood vessels are sealed. As a result, the liquid and blood stops sweating under the retina and peeling it off, which stops the progression of the disease. Laser coagulation of blood vessels is a short and completely painless procedure that can be performed in a polyclinic.

After laser coagulation, it is necessary to take drugs from the group of angiogenesis inhibitors, for example, Lucentis, which will inhibit the active growth of new, abnormal vessels, thereby stopping the progression of wet macular degeneration of the retina. Lucentis should be taken continuously, and other medicines - courses several times a year, as with dry macular degeneration.

Principles of treatment of peripheral retinal dystrophy

Retinal dystrophy - laser treatment

Examples of therapeutic treatment of dystrophy with a laser are retinal stimulation, during which the affected areas are irradiated in order to activate metabolic processes in them. Laser stimulation of the retina in most cases gives an excellent effect and allows you to stop the progression of the disease for a long time. An example of surgical laser treatment of dystrophy is vascular coagulation or delimitation of the affected area of ​​the retina. In this case, the laser beam is directed to the affected areas of the retina and, under the influence of the released thermal energy, literally sticks together, seals the tissues and, thereby, delimits the treated area. As a result, the area of ​​the retina affected by dystrophy is isolated from other parts, which also makes it possible to stop the progression of the disease.

Retinal dystrophy - surgical treatment (surgery)

Vitamins for retinal dystrophy

Vitamins for retinal dystrophy must be taken in two forms - in special tablets or multivitamin complexes, as well as in the form of foods rich in them. The richest in vitamins A, E and group B are fresh vegetables and fruits, cereals, nuts, etc. Therefore, these products must be consumed by people suffering from retinal dystrophy, as they are sources of vitamins that improve the nutrition and functioning of the eyes.

Prevention of retinal dystrophy

• Do not strain your eyes, always let them rest;
• Do not work without eye protection from various harmful radiation;
• Do gymnastics for the eyes;
• Eat well, including fresh vegetables and fruits in the diet, as they contain a large amount of vitamins and minerals necessary for the normal functioning of the eye;
• Take vitamins A, E and group B;
• Take a zinc supplement.

Retinal dystrophy - folk remedies

The retina is a thin membrane lining the fundus of the eye from the inside. It has a multilayer structure. On the one hand, it is attached to the choroid, on the other - to the vitreous body. The retina is involved in the processing of information coming through the visual organs, and conducts this information to the brain. Retinal diseases reduce the quality of human life, as they lead to deterioration of vision, in advanced stages lead to its complete loss.

What is retinal detachment

Retinal detachment occurs when the membranes of the eye, vascular and retinal, for various reasons, begin to delaminate among themselves. The process begins with partial delamination and can reach complete delamination of the shells from each other.

A retinal detachment does not cause instant blindness. The process of stratification can proceed for several days or even weeks, so a person has the opportunity to stop it. When seeking medical help, there is a high probability of complete preservation of the visual functions of the eye.

A characteristic sign of detachment of the retina is the so-called. Weiss ring. This is a condition when a person sees a circle in front of the affected eye, around which there is a clouding of the image. Before the eyes, there is always, as it were, a fog or a veil of varying degrees of density, some areas fall out of the field of vision of a person and form blind zones. These signs are observed in the evenings and are absent in the morning.

Causes of pathology

The causes of retinal detachment are usually divided into 2 groups:

1. Primary.
2. Secondary.

The primary group of detachment is characterized by rupture of the retina and accumulating fluid in places where the rupture occurred.

The secondary group is associated with the occurrence of neoplasms, both benign and oncological.

Many factors affect retinal detachment, the causes of this disease may be the following:

• diseases of the circulatory system;
• stress, short-term or permanent;
• viral diseases and infections;
• myopia;
• consequences of ophthalmic operations;
• thinning and dystrophy of the retina;
• pregnancy and childbirth;
• excessive physical and emotional stress;
• diabetes mellitus of both types;
• thinning of the mucous membranes, characteristic of the elderly;
• traumatic head and eyeball injuries.

Symptoms of the disease

Retinal detachment and its signs can be tracked independently. Any deterioration in the visual process that does not go away within a day or more requires immediate consultation with a specialist. With retinal detachment, the symptoms of the disease will be as follows:

• before the eyes there is always a fog or a veil of varying degrees of density;
• shadows are constantly observed at the edges of the field of view, which sway if a person moves his head;
• small black dots are constantly present in the field of view;
• sensation of explosions of light in the eyeball, from the side closest to the temple;
• curvature of familiar shapes and lines when looking at familiar objects;
• appearance of the Weiss ring.

The described signs are noticed by people in the evening. In the morning, patients practically do not track them, since the fluid that has accumulated at night in places where the separation has begun has time to resolve naturally. Patients even have a slight improvement in vision in the morning. Because of this, few people immediately seek the advice of an ophthalmologist. Therefore, the area of ​​stratification grows, and the disease quickly passes into a more severe and irreversible form.

Diagnosis and treatment

If a retinal dissection is suspected, a complete ophthalmological examination should be performed immediately. This is the only way to preserve vision and avoid complete blindness.

When examining visual functions, visual acuity is checked, the field of view and the presence of blind spots in them are determined in the patient. All data are obtained using perimetry: static, kinetic or computer. The disappearance of previously visible zones from the viewing circle is associated with the beginning of the process of shell delamination. Blind spots appear on the side of the eye opposite the one where the detachment began.

Biomicroscopy is performed to examine the fundus and detect pathologies in the vitreous body. The intraocular pressure is measured in both eyeballs. In the eye, where there is a separation of the membranes, the pressure is always lower than in a healthy eyeball.

Ophthalmoscopy is one of the most important studies for determining the condition of the visual organs. This study allows you to most fully identify the size and degree of damage that appeared as a result of delamination. These data help to determine the number of breaks, their area and location, the state of the vitreous body and the presence of pathologies in it. This examination allows you to identify areas with retinal dystrophy, which is necessary for surgical operations.

There are cases when it is necessary to refuse ophthalmoscopic examination. This happens when the lens or vitreous body becomes cloudy. Then the patient is required to conduct an ultrasound examination of the eyeball.

An electrophysiological study is used to assess the condition of the retina, its viability and the presence of problems in the optic nerve.

Treatment of retinal detachment is carried out by surgical intervention. There are 2 types of such operations:

1. Extrascleral. The operation is performed on the surface of the sclera. These techniques include operations for sealing and ballooning the sclera.
2. Endovital. They are carried out inside the eyeball.

In cases where extrascleral filling is used, a specially designed silicone filling is used. It is attached to the sclera, provides the effect of the necessary pressure on its surface. The filling helps to block retinal tears and removes fluid that has accumulated there.

Ballooning of the scleral surface is performed by temporarily fixing a special balloon catheter into the area of ​​the rupture, which can be inflated. Its effect is similar to the action of a filling - the process of blocking gaps occurs and the accumulation of fluid is removed.

Treatment using endovitreal methods is performed using vitrectomy. During this operation, the damaged vitreous body is removed. Instead, special preparations are introduced that help bring together and press the exfoliated reticular and choroid membranes together.

There are also more lightweight methods for treating retinal detachment. With ruptures and detachment of the retina, laser coagulation and cryocoagulation can be used. These techniques allow the formation of special medical adhesions to prevent further ruptures.

Forecast and prevention

The prognosis in the case when retinal detachment is detected is associated with the moment the pathology is detected. If the pathology is detected at the very beginning of the disease, the operation is performed on time, then the patient has every chance that the vision will remain at the same level.

With a careful attitude to one's own health, retinal detachment can be avoided. People registered with diabetes mellitus, having traumatic injuries of the head and eyes, patients with myopia, suffering from retinal dystrophy, pregnant women, suffering from various eye diseases, need a constant preventive examination by an ophthalmologist. Such people are contraindicated in heavy physical and emotional stress.

(M.V. Lipkin. Visual system. Mechanisms of transmission and amplification of the visual signal in the retina. Soros Educational Journal. 2001. Volume 7, No. 9. P.2-8)

V.M. Lipkin, Pushchino State University

Sight is one of the most delightful gifts that nature has bestowed on man. With the help of vision, we receive a huge amount of information about the state of the environment, we can enjoy the beauties of nature and the great works of culture and art. Vision is necessary for a person both in the process of his professional activity and on vacation, from morning until late in the evening. Even in a dream, previously seen visual images are realized in the human brain during dreams.

Basic elements of the visual system

When we look at the world around us, its image is initially focused on the retina of each of the two eyes. The retina is a part of the brain that separated from it in the early stages of vertebrate evolution, but is still connected to it through a bundle of nerve cells - the optic nerve (Fig. 1). The retina contains 125 million light-sensitive cells called rods and cones, which are specialized to generate electrical signals in response to light impulses. From the retina, an electrical signal is transmitted along the optic nerve to a specialized cell cluster located deep in the brain, the so-called external (lateral) geniculate body. Then it enters the visual cortex, located in the back of the brain. Initially, information enters the primary visual zone, from where, after passing through several layers of synaptically connected cells, it is transmitted to neighboring higher order zones, where, ultimately, the image of the object we are looking at is formed.

Retina

Rice. 1. Structural elements of the human visual system. An enlarged fragment of the retina shows the relative position of its three layers (Montgomery G. Breaking the Code of Color // Seeing, Hearing, and Smelling the World: A Report from the Howard Hughes Medical Institute. 1995. P. 15)

The most important structure of the visual system of animals is the retina. The retina converts light into nerve signals, allowing us to see from a starry night to a sunny day, distinguishes wavelengths that enable us to see colors, and is accurate enough to spot a human hair or speck from several meters away. In humans, the retina is shaped like a plate about a quarter of a millimeter thick and consists of three layers of nerve cell bodies separated by two layers of synapses. The layer of cells on the back of the retina contains light-sensitive receptors: rods and cones. Rods, much more numerous than cones (in humans, there are approximately 120 million rods and about 7 million cones per retina), are responsible for our vision in low light and turn off in bright light. Cones function only in bright light, they are responsible for the ability to see fine details and color vision. Most of the cones are concentrated in the central area of ​​the retina with a diameter of about half a millimeter, called the fovea. Both types of photoreceptors are long, narrow cells. They got their name because of the shape of their outer segments, which are thin, cylindrical in rods, and much more thickened in cones.

Moving from the back layer of the retina to the front, we get into the middle layer, located between the rods and cones, on the one hand, and the ganglion cells, on the other. This layer contains three types of neurons: bipolar, horizontal, and amacrine cells. Bipolar cells have inputs from receptors, as shown in Fig. 1. Horizontal cells connect receptors and bipolar cells with relatively long bonds running parallel to the retinal layers. Similarly, amacrine cells connect bipolar cells to ganglion cells. The layer of neurons on the anterior side of the retina contains ganglion cells, whose axons travel along the surface of the retina, gathering in a bundle, and leaving the eye, forming the optic nerve (see Fig. 1). There are two ways of information flow through the retina: a direct way from photoreceptors to bipolar cells and further to ganglion cells, and an indirect way, in which horizontal cells are included between receptors and bipolars, and amacrine cells between bipolars and ganglion cells. The direct path is very specific and compact, mainly realized by signal transmission from the fovea and provides sharp vision. The indirect path is more diffuse or blurred due to wide lateral connections and is realized mainly in the peripheral areas of the retina.

The most important process in the functioning of the retina is the conversion of absorbed light into an electrical signal, which is carried out in photoreceptor cells. Before proceeding to a description of the mechanism of this process, let us consider in general terms the structure of rods and cones.

Photoreceptors

Rods are highly specialized nerve cells that have specialized processes (outer segments), the endings of which face the outer surface of the retina. Rod outer segments (ERS) of vertebrates contain a stack of hundreds or even thousands of so-called photoreceptor discs (Fig. 2). The discs form at the base of the NSP as an invagination of the plasma membrane, with the inner space of the newly formed discs still communicating with the extracellular space. Later, the disks, as it were, bud off from the plasma membrane, turning into closed structures, and become independent both from it and from each other. Thus, the outer surface of the plasma membrane turns out to be the inner surface of the discs, and their lumen originates from the extracellular space.

The outer segments of cones have a fundamental difference from the NSP, which consists in the fact that cone discs are folds of the plasma membrane and their intracellular space communicates with the extracellular environment.

Rice. 2. Scheme of activation of the visual cascade:

• I - in the dark state, rhodopsin is inactive (R). a-subunit of transducin (T) is complexed with GDP (Ta-GDP) and is associated with a dimer of b- and g-subunits (Tbg). cGMP-phosphodiesterase (PDE) is a heterotetramer consisting of two homologous catalytic a- and b-subunits (PDEab) and two identical g-subunits (PDEg), which are intramolecular enzyme inhibitors, and is inactive. Guanylate cyclase maintains a high level of cGMP in the cytoplasm. cGMP-dependent cation channels in the plasma membrane are open, and Na + and Ca 2+ cations can diffuse from the extracellular space into the cytosol. The intracellular Ca 2+ concentration is maintained at a constant level by the Na + /Ca 2+ , K + -cation exchanger located in the plasma membrane;
• II - as a result of the absorption of a light quantum, rhodopsin passes into an active state (R -> R *). Active R* binds to transducin and induces the exchange of Ta-bound GDP for GTP;
• III – the R*-(Ta -GTP)-Tbg complex dissociates into R*, T and the active T*a -GTP complex, after which R* is able to activate another transducin molecule;
• IV - T*a -GTP activates PDE. The activated phosphodiesterase PDE*ab hydrolyzes many cGMP molecules. A decrease in the intracellular concentration of cGMP leads to the closure of cGMP-dependent channels, which leads to hyperpolarization of the plasma membrane.

On the left is a schematic representation of the retinal rod

Both rods and cones contain light-sensitive pigments - light receptors. In all human rods the pigment is the same; cones are divided into three types, each with its own special visual pigment. These four pigments are sensitive to different wavelengths of light, and in the case of cones, these differences form the basis of color vision. In rods, most of the visual pigment (called rhodopsin) is located in the membrane of the photoreceptor discs. Under the influence of light, the rhodopsin molecule absorbs a single quantum of visible light (photon), which leads to a chemical restructuring of the visual receptor.

In the plasma membrane of the NSP (outer segment of the rods) of vertebrates, separated from the disc membrane, there are special cyclic guanosine monophosphate (cGMP) dependent cation channels specific for Na + and Ca 2+ . In the dark, some of these channels are open, and Na + and Ca 2+ cations can freely diffuse from the extracellular space into the cytosol. The flow of ions in the dark or dark current, discovered in 1970 by William Hagins, causes depolarization (reduction of the external positive charge) of the NSP plasma membrane. In the dark, the NSP membrane potential is approximately 50 mV instead of the usual 70 mV for a normal nerve cell. Thus, in the dark, vertebrate photoreceptors are more depolarized than normal resting nerve cells, and the depolarization causes a continuous release of transmitter from their axon endings, just as happens in normal receptors when stimulated. Most sensory receptors - chemical, temperature or mechanical - in response to the appropriate stimulus, the cell membrane depolarizes, that is, they behave in the same way as ordinary neurons.

As a result of the absorption of a quantum of light by the rhodopsin molecule and the subsequent biochemical reactions, the cationic (Na + /Ca 2+) channels are closed, which leads to a decrease in the dark current and hyperpolarization (increase in the external positive charge) of the plasma membrane of the cell. Light, increasing the potential on the membrane of the receptor cell (hyperpolarizing it), reduces the release of the mediator. Thus, stimulation, oddly enough at first glance, turns off the receptors. The processes of perception, transmission and amplification of the visual signal, called phototransduction, are actively studied in many laboratories. The main question is how light causes hyperpolarization of the receptor cell membrane and, in particular, how the absorption of a single photon by just one molecule of rhodopsin can lead to a noticeable change in the membrane potential and the act of photoreception. The human eye, after appropriate dark adaptation, is able to register individual light quanta, that is, its sensitivity reaches the theoretical limit. The following sections of the article summarize the latest advances in the study of the molecular mechanisms of phototransduction in photoreceptor cells. These processes involve a significant number of protein components, the totality of which is usually called the visual cascade.

visual cascade

On fig. 2 shows the main components of the system of perception, transmission and amplification of the visual signal in rods of vertebrates and the main biochemical reactions in which they take part. The first step of the phototransduction process is the absorption of a light quantum by the photoreceptor pigment, rhodopsin, and the transition of rhodopsin to the photoactivated state (R -> R*). Rhodopsin is a glycoprotein with a molecular weight of about 40 kDa, consisting of an opsin protein and a chromophore covalently bound to it (l max rhodopsin = 498 nm). The universal chromophore in the rods and cones of the vertebrate retina and in the photoreceptors of invertebrates is 11 cis-retinal. Opsin is an integral membrane protein that accounts for about 70% of the total ESP (rod outer segment) protein and is localized in disc membranes and the ESP plasma membrane. At the same time, rhodopsin-containing regions of the plasma membrane of the NSP are the precursors of newly formed discs. Rhodopsin belongs to the family of G-protein-coupled receptors (G-proteins are proteins that can bind guanyl nucleotides GDP and GTP and take part in the transmembrane transmission of various signals). The mechanism of the initial stages of the phototransduction process is similar to the mechanism of transmembrane signaling involving receptors of this family (for more details, see ).

The absorption of a quantum of light by rhodopsin leads to a number of its photochemical transformations - photolysis. The primary act in this process is the isomerization of 11- cis- retinal in full trance-shape (Fig. 3). Retinal isomerization is the only light-dependent process during the light activation of rhodopsin, all other stages of photolysis are light-independent, they are associated with conformational rearrangements in the opsin molecule and protonation–deprotonation reactions of the Schiff base formed between retinal and the e-amino group of the lysine-296 residue of opsin (Schiff bases are compounds , formed as a result of the reaction of an aldehyde and an amine, accompanied by the elimination of water, and having a C=N double bond). About 200 femtoseconds elapse between the absorption of a photon and the isomerization of retinal. This event is followed by the formation within milliseconds of several intermediate forms of rhodopsin, each of which is characterized by its own absorption spectrum. One of the intermediates of rhodopsin photolysis, metarhodopsin II (l max = 380), which contains a non-protonated Schiff base with completely trance-retinal and is characterized by significant conformational rearrangements in comparison with dark rhodopsin.

Rice. 3. Isomerization of chromophore 11- cis- retinal in full trance- retinal as a result of the absorption of a quantum of light by a molecule of visual pigment (rhodopsin)

Metarhodopsin II (R*) acts as a catalyst in the process of activation of the next visual cascade protein, transducin (T). Transducin belongs to the family of heterotrimeric G proteins and consists of alpha, beta, and gamma subunits (Ta, Tb, and Tg) with molecular weights of 40, 37, and 8 kDa, respectively. The Tb and Tg subunits are tightly bound to each other and function as a single Tbg subunit. The most important characteristic of transducin, like all G-proteins, is the presence on their a-subunit of the binding site for guanyl nucleotides: GDP and GTP. In the dark (Fig. 2, I), Ta is complexed with the GDP molecule (Ta -GDP) and is bound to the Tbg dimer. The (Ta-GDP)-Tbg complex is localized on the outer surface of the disk membrane and has an increased affinity for metarhodopsin II. The binding of R* to (Ta-GDP)-Tbg induced the exchange of Ta-bound GDP for GTP (Fig. 2, II). The R*-(Ta -GDP)-Tbg complex rapidly dissociates into R*, the active Ta*-GTP complex, and Tbg. The released R* is able to activate another transducin molecule (Fig. 2, III). Activation of hundreds or even thousands of transducin molecules by a single photoexcited rhodopsin molecule is the first amplification step in the process of visual signal transmission.

T*a -GTP, in turn, activates the next visual cascade protein, cyclic GMP phosphodiesterase (PDE) (cGMP). PDE from NSP is a peripheral membrane protein (localized on the surface of disks) with a molecular weight of about 220 kDa, consisting of four subunits: two homologous PDEa - and PDEb - subunits (molecular weights 99 and 98 kDa) and two identical PDEg -subunits (10 kDa each). The PDEa- and PDEb-subunits perform the catalytic function of the cGMP hydroface, and the PDEg-subunit is an internal inhibitor of the enzyme.

By analogy with other G-protein-coupled receptor systems, in the rhodopsin–transducine-phosphodiesterase cGMP system, PDE is the effector protein, and cGMP is the second messenger. However, unlike most receptor systems, which serve to transmit a signal from the outside of the cell membrane into the cell, visual cascade proteins transmit a signal from the disk membrane located inside the NSP to the outer plasma membrane. Let's consider this process in more detail. In the dark, PDE is inactive, and a high level of cGMP is maintained in the rod cytoplasm due to the activity of the guanylate cyclase enzyme. As a result, most of the cGMP-dependent cationic (Na + /Ca 2+) channels in the NSP plasma membrane are in the open state, and Na + and Ca 2+ cations freely diffuse from the extracellular space into the cytosol (see Fig. 2, I) which leads to depolarization of the plasma membrane. Na + cations penetrating into the cytoplasm are removed from the cell by Na + /K + - ATPase located in the body of the rod (inner segment). The intracellular Ca 2+ concentration is maintained at a constant level by the NSP Na + /Ca 2+ , K + -cation exchanger located in the plasma membrane.

Interacting with PDE, T*a -GTP removes the inhibitory effect of PDEg on the enzyme (Fig. 2, IV), while complete activation of PDE requires the presence of two T*a -GTP molecules per enzyme molecule (one for each PDEg subunit) . Activated phosphodiesterase (PDE*) hydrolyzes many cGMP molecules (up to three thousand molecules per molecule of active enzyme), and this process is the second step in enhancing the visual signal (the total amplification factor reaches 10 5 -10 6). A decrease in the intracellular concentration of cGMP leads to the closure of cGMP-dependent cation channels and hyperpolarization of the plasma membrane (see Fig. 2, IV). Thus, the photoreceptor pigment rhodopsin is responsible for the perception of the visual signal in the NSP. Four proteins are involved in signal transduction to the plasma membrane: rhodopsin, transducin, phosphodiesterase cGMP, and cGMP-dependent cation channel, while cGMP, being a second messenger, directly transmits the signal from the disc membrane to the outer plasma membrane. The role of cGMP as a second messenger in visual signal transmission was first proven by E.E. Fesenko (Institute of Cell Biophysics, Russian Academy of Sciences). The electrophysiological response of a photoreceptor cell to a light stimulus lasts for hundreds of milliseconds and then stops due to the existence in the NSP of mechanisms responsible for turning off the phosphodiesterase cascade and restoring the dark state.

OFF THE VISUAL CASCADE

After closing cGMP-dependent channels in the cytoplasm of the bacillus, as a result of the activity of Na + /Ca 2+ , K + - cation exchanger, the concentration of Ca 2+ cations decreases. Switching off the visual cascade occurs as a result of a successive series of reactions (Fig. 4) and is directly related to a decrease in the intracellular concentration of Ca 2+ cations. The first reaction in this process is R* phosphorylation, which significantly reduces the ability of the pigment to activate transducin. Rhodopsin kinase, a protein with a molecular weight of 67 kDa, is responsible for R* phosphorylation in NSP. Rhodopsinkinase phosphorylates only photoactivated R* and does not interact with rhodopsin in the dark. The activity of rhodopsin kinase is regulated by a Ca 2+ -dependent manner with the help of a Ca 2+ -binding protein, recoverin. In the dark, at a high Ca2+ concentration, recoverin prevents unwanted pigment phosphorylation, while a decrease in the Ca2+ concentration leads to the activation of rhodopsin kinase (Fig. 4, II). Phosphorylated R* (R*–P) has an increased affinity for another protein, arrestin. Binding of arrestin leads to complete loss of the ability (R*–P) to activate transducin. Thus, inactivation of rhodopsin requires its phosphorylation and interaction with arrestin. Inactivation of T*a-GTP occurs as a result of the hydrolysis of bound GTP to GDP, Ta itself having the ability to hydrolyze GTP (GTPase activity). However, the rate of spontaneous hydrolysis is rather slow. It increases with the interaction of T*a -GTP with PDEg, as well as with a decrease in the level of cGMP in the NSP. Recently, the so-called RGS-protein belonging to the class of G-proteins has been discovered, which, interacting with T*a -GTP, dramatically increases the rate of GTP hydrolysis. After GTP hydrolysis, Ta-GDP rapidly dissociates from PDEg, and the association of PDEg with PDE*ab leads to enzyme inactivation (see Fig. 4, II). The association process (Ta-GDP) with Tbg is controlled by another protein, fosducin.

Rice. 4. Scheme of turning off the visual cascade and returning the photoreceptor to the dark state:

• I is the photoactivated state of the NSP. Molecules of rhodopsin, transducin and cGMP phosphodiesterase are in an active state. cGMP-dependent channel is closed;
• II - as a result of the activity of Na + /Ca 2+ , K + -cation exchanger, the intracellular concentration of Ca cations decreases. A decrease in Ca 2+ concentration leads to the activation of rhodopsin kinase (RK—>RK*), which phosphorylates photoexcited R*. Phosphorylated rhodopsin (R*~P) binds strongly to arrestin (Ar), which blocks the site of interaction between rhodopsin and transducin and thus prevents further formation of T*a -GTP . T*a -GTP is inactivated as a result of hydrolysis of GTP to GDP due to the internal GTP-ase activity of Ta and Ta -GDP dissociates from PDEg. PDEg associates with PDE catalytic subunits (PDE*ab ) and inactivates the enzyme;
• III - the concentration of cGMP increases to the dark level due to the activation of gunylate cyclase (GC*), which occurs as a result of a decrease in the concentration of Ca 2+ . The cGMP-dependent cation channel opens, resulting in depolarization of the plasma membrane. Phosphatase 2A (P2A) dephosphorylates R*~P. Dephosphorylated rhodopsin breaks down completely trance- retinal and opsin;
• IV - opsin covalently attaches 11- cis-retinal with the formation of rhodopsin. The photoreceptor cell returns to its original dark state

A decrease in the level of free calcium in the cytoplasm of the NSP, caused by light, also leads to the activation of guanylate cyclase (GC*), the enzyme responsible for restoring the dark level of cGMP. The action of Ca on GC in photoreceptors is mediated by the regulatory GC-activating protein (GCAP). GCAP does not affect the basal activity of GC in the presence of Ca 2+ , but increases its activity with a decrease in the concentration of the latter. A decrease in Ca 2+ concentration also affects the activity of the cGMP-dependent cation channel, and this effect is mediated by another Ca 2+-binding protein, calmodulin. Thus, the process of turning off the visual signal is controlled by three Ca2+-binding proteins: recoverin, GCAP, and calmodulin.

The return of the photoreceptor to the dark state

As a result of a decrease in the concentration of Ca2+ and a subsequent increase in the concentration of cGMP in the cytoplasm of the NSP, cGMP-dependent cation channels open (Fig. 4, III) and the dark current is restored, which leads to depolarization of the photoreceptor. The most difficult process in the process of returning the photoreceptor to the dark state is the restoration of the photosensitivity of rhodopsin. The slowest reaction is the breakdown of the arrestin complex with phosphorylated rhodopsin, which begins with complete dissociation trance-retinal. Further, the free phosphorylated opsin is dephosphorylated with the help of phosphatase 2A (Fig. 4, III), after which, finally, the regeneration of rhodopsin becomes possible as a result of the binding of opsin to 11- cis-retinal (Fig. 4, IV).

CONCLUSION

A large number of various protein molecules, which are in dynamic interaction with each other, take part in phototransduction processes. The nature of these interactions is entirely determined by the primary and spatial structure of the interacting proteins. In this case, the interaction of proteins underlies both the mechanisms of activation and deactivation of the visual cascade and the mechanisms of returning the photoreceptor to the dark state.

LITERATURE

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Reviewer of the article A.Ya. Potapenko

Valery Mikhailovich Lipkin, doctor of chemical sciences, professor, head. Department of Protein Engineering, Pushchino State University, Deputy. director of the Institute of Bioorganic Chemistry. MM. Shemyakin and Yu.A. Ovchinnikov RAS, Corresponding Member of the RAS, laureate of the USSR State Prize and the Prize. Yu.A. Ovchinnikov. The area of ​​scientific interests is the structure and function of protein molecules. Author of 180 scientific papers, including two monographs.