How to restore the myelin sheath of nerve fibers. Shirokov E.A.

MYELIN DIET The myelin sheath helps nerves transmit signals. If it is damaged, memory problems arise, often a person has specific movements and functional disorders . Certain autoimmune diseases and environmental chemicals, such as pesticides in food, can damage the myelin sheath. But there are a number of ways, including vitamins and food, to help regenerate this nerve coating: you need specific minerals and fats, preferably from a nutritious diet. This is all the more necessary if you are suffering from a disease such as multiple sclerosis: usually the body is able to repair the damaged myelin sheath with some help from you, but if sclerosis has manifested, treatment can become very difficult. So, here are the remedies that will help support the repair and regeneration of the myelin sheath, as well as prevent multiple sclerosis. So, here are the remedies that will help support the repair and regeneration of the myelin sheath, as well as prevent multiple sclerosis. You will need: - folic acid; - vitamin B12; - essential fatty acids; - vitamin C; - vitamin D; - green tea; - martinia; - white willow; - boswellia; - olive oil; - fish; - nuts; - cocoa; - avocado; - whole grains; - legumes; - spinach. Actions: 1. Provide yourself with folic acid and vitamin B12 supplements. The body needs these two substances in order to protect the nervous system and to properly “repair” the myelin sheaths. In a study published in the Russian medical journal Vrachebnoe delo in the 1990s, scientists found that patients suffering from multiple sclerosis who were treated with folic acid showed significant improvement in symptoms and in terms of myelin repair. Both folic acid and B12 can both help prevent breakdown and regenerate damage to myelin. 2. Reduce inflammation in the body to protect myelin sheaths from damage. Anti-inflammatory therapy is currently the mainstay of multiple sclerosis treatment and in addition to taking prescribed medications, patients can also try dietary and herbal anti-inflammatory agents. Among natural remedies, essential fatty acids, vitamin C, vitamin D, green tea, martinia, white willow and boswellia are noted. 3. Consume essential fatty acids daily. The myelin sheath is primarily made up of an essential fatty acid: oleic acid, an omega-6 found in fish, olives, chicken, nuts, and seeds. Plus, eat deep sea fish for a good amount of omega-3s for improved mood, learning, memory, and overall brain health. Omega-3 fatty acids reduce inflammation in the body and help protect myelin sheaths. Fatty acids can also be found in flaxseed, fish oil, salmon, avocados, walnuts and beans. The myelin sheath is mainly composed of an essential fatty acid: oleic acid, an omega-6 found in fish, olives, chicken, nuts, and seeds 4. Maintain immune system. The inflammation that causes damage to the myelin sheaths is caused by immune cells and autoimmune diseases of the body. Nutrients that help with immunity include: vitamin C, zinc, vitamin A, vitamin D, and vitamin B complex. In a 2006 study published in The Journal of the American Medical Association, vitamin D has been named as a tool that significantly helps to reduce the risk of demyelination and manifestations of multiple sclerosis. 5. Eat foods high in choline (vitamin D) and inositol (inositol; B8). These amino acids are critical for the repair of myelin sheaths. Choline is found in eggs, beef, beans, and some nuts. It helps prevent fat deposits. Inositol Supports Health nervous system by assisting in the creation of serotonin. Nuts, vegetables and bananas contain inositol. The two amino acids combine to produce lecithin, which reduces the "bad" fats in the bloodstream. Well, cholesterol and similar fats are known for their ability to prevent the restoration of myelin sheaths. 6. Eat foods rich in B vitamins. Vitamin B-1, also called thiamine, and B-12 are the physical components of the myelin sheath. We are looking for B-1 in rice, spinach, pork. Vitamin B-5 can be found in yogurt and tuna. Whole grains and dairy products are rich in all of the B vitamins, and they can also be found in whole grain bread. These nutrients increase the metabolism that burns fat in the body, and they also carry oxygen. 7. You also need food containing copper. Lipids can only be created using copper dependent enzymes. Without this help, other nutrients won't be able to do their job. Copper is found in lentils, almonds, pumpkin seeds, sesame seeds and semi-sweet chocolate. Liver and seafood may also contain copper at lower levels. Dry herbs like oregano and thyme are an easy way to add this mineral to your diet. Additions and warnings: - Milk, eggs and antacids can interfere with the absorption of copper; - In culinary recipes, change olive oil to solid oil (this happens too!); - If you drink too many B vitamins, they will simply leave the body without harming it; - An overdose of copper can cause serious problems of the mind and body. So the natural consumption of this mineral is the best option; - Even natural methods, such as food selection and other things, should be supervised by a doctor.

Demyelination Demyelination is a disease caused by selective damage to the myelin sheath that runs around nerve fibers

Demyelination- a pathological process in which myelinated nerve fibers lose their insulating myelin layer. Myelin, phagocytosed by microglia and macrophages, and subsequently by astrocytes, is replaced by fibrous tissue (plaques). Demyelination disrupts impulse conduction along the conduction pathways of the white matter of the brain and spinal cord; peripheral nerves are not amazed.

DEMYELINIZATION - destruction of the myelin sheath of nerve fibers as a result of inflammation, ischemia, trauma, toxic-metabolic or other disorders.

Demyelination is a disease caused by selective damage to the myelin sheath that surrounds the nerve fibers of the central or peripheral nervous system. This, in turn, leads to dysfunction of myelinated nerve fibers. Demyelination may be primary (eg, multiple sclerosis), or develops after a skull injury.

DEMYELINATING DISEASES

Diseases, one of the main manifestations of which is the destruction of myelin, is one of the most pressing problems. clinical medicine, predominantly neuroscience. AT last years there is a clear increase in the number of cases of diseases accompanied by damage to myelin.

myelin - special kind cell membrane surrounding the processes of nerve cells, mainly axons, in the central (CNS) and peripheral nervous system (PNS).

The main functions of myelin:
axon nutrition
isolation and acceleration of nerve impulse conduction
support
barrier function.

By chemical composition myelin is a lipoprotein membrane consisting of a biomolecular lipid layer located between monomolecular layers of proteins, spirally twisted around the internodal segment of the nerve fiber.

Myelin lipids are represented by phospholipids, glycolipids and steroids. All these lipids are built according to a single plan and necessarily have a hydrophobic component ("tail") and a hydrophilic group ("head").

Proteins make up to 20% of the dry mass of myelin. They are of two types: proteins located on the surface, and proteins immersed in the lipid layers or penetrating the membrane through. In total, more than 29 myelin proteins have been described. Myelin basic protein (MBP), proteolipid protein (PLP), myelin-associated glycoprotein (MAG) account for up to 80% of the protein mass. They perform structural, stabilizing, transport functions, have pronounced immunogenic and encephalitogenic properties. Among the small proteins of myelin Special attention deserves myelin-oligodendrocyte glycoprotein (MOG) and myelin enzymes having great importance in maintaining structural-functional relationships in myelin.

CNS and PNS myelins differ in their chemical composition
in the PNS, myelin is synthesized by Schwann cells, with several cells synthesizing myelin for a single axon. One Schwann cell forms myelin for only one segment between areas without myelin (nodes of Ranvier). Myelin in the PNS is noticeably thicker than in the CNS. All peripheral and cranial nerves have such myelin, only short proximal segments cranial nerves and spinal roots contain CNS myelin. The optic and olfactory nerves contain predominantly central myelin
in the CNS, myelin is synthesized by oligodendrocytes, with one cell taking part in the myelination of several fibers.

Myelin destruction is a universal mechanism for the response of nervous tissue to damage.

Myelin diseases fall into two main groups.
myelinopathy - associated with a biochemical defect in the structure of myelin, as a rule, genetically determined

Myelinoclasia - the basis of myelinoclastic (or demyelinating) diseases is the destruction of normally synthesized myelin under the influence of various influences, both external and internal.

The division into these two groups is very conditional, since the first clinical manifestations myelinopathy may be associated with exposure to various external factors, and myelinoclasts are more likely to develop in predisposed individuals.

The most common disease of the entire group of myelin diseases is multiple sclerosis. It is with this disease that differential diagnosis is most often made.

hereditary myelinopathies

The clinical manifestations of most of these diseases are more often observed already in childhood. At the same time, there are a number of diseases that can begin at a later age.

Adrenoleukodystrophy (ALD) are associated with insufficiency of the function of the adrenal cortex and are characterized by active diffuse demyelination of various parts of both the central nervous system and the PNS. The main genetic defect in ALD is associated with the Xq28 locus on the X chromosome, the genetic product of which (ALD-P protein) is a peroxisomal membrane protein. The type of inheritance in typical cases is recessive, sex-dependent. Currently, more than 20 mutations have been described at different loci associated with different clinical options ALD.

The main metabolic defect in this disease is an increase in the content of saturated fatty acids with a long chain (especially C-26), which leads to gross violations of the structure and functions of myelin. Along with the degenerative process in the pathogenesis of the disease, chronic inflammation in the brain tissue associated with increased production of tumor necrosis factor alpha (TNF-a) is essential. The ALD phenotype is determined by the activity of this inflammatory process and is most likely due to both a different set of mutations on the X chromosome and an autosomal modification of the effect of a defective genetic product, i.e. a combination of a basic genetic defect in the sex X chromosome with a peculiar set of genes on other chromosomes.

The nervous system performs the most important functions in the body. It is responsible for all actions and thoughts of a person, forms his personality. But all this complex work would not be possible without one component - myelin.

Myelin is a substance that forms the myelin (pulp) sheath, which is responsible for the electrical insulation of nerve fibers and the speed of transmission of electrical impulses.

Anatomy of myelin in the structure of the nerve

The main cell of the nervous system is the neuron. The body of a neuron is called the soma. Inside it is the core. The body of a neuron is surrounded by short processes called dendrites. They are responsible for communicating with other neurons. One long process departs from the soma - the axon. It carries an impulse from a neuron to other cells. Most often, at the end, it connects to the dendrites of other nerve cells.

The entire surface of the axon is covered by the myelin sheath, which is a process of the Schwann cell devoid of cytoplasm. In fact, these are several layers of the cell membrane wrapped around the axon.

The Schwann cells that envelop the axon are separated by nodes of Ranvier, which lack myelin.

Functions

The main functions of the myelin sheath are:

• axon isolation;
• acceleration of impulse conduction;
• energy savings due to the conservation of ion flows;
• support of the nerve fiber;
• axon nutrition.

How impulses work

Nerve cells are isolated due to their shell, but still interconnected. The sites where cells touch are called synapses. This is the place where the axon of one cell and the soma or dendrite of another meet.

An electrical impulse can be transmitted within a single cell or from neuron to neuron. This is a complex electrochemical process, which is based on the movement of ions through the shell nerve cell.

In a calm state, only potassium ions enter the neuron, while sodium ions remain outside. At the moment of excitement, they begin to change places. The axon is positively charged internally. Then sodium ceases to flow through the membrane, and the outflow of potassium does not stop.

The change in voltage due to the movement of potassium and sodium ions is called an "action potential". It spreads slowly, but the myelin sheath that envelops the axon accelerates this process by preventing the outflow and inflow of potassium and sodium ions from the axon body.

Passing through the interception of Ranvier, the impulse jumps from one section of the axon to another, which allows it to move faster.

After the action potential crosses the gap in myelin, the impulse stops and the resting state returns.

This mode of energy transfer is characteristic of the CNS. In the autonomic nervous system, axons are often found covered with little or no myelin. Jumps between Schwann cells are not carried out, and the impulse passes much more slowly.

Compound

The myelin layer consists of two layers of lipids and three layers of protein. There are much more lipids in it (70-75%):

• phospholipids (up to 50%);
• cholesterol (25%);
• glaktocerebroside (20%), etc.

The protein layers are thinner than the lipid ones. The protein content in myelin is 25-30%:

• proteolipid (35-50%);
• myelin basic protein (30%);
• Wolfgram proteins (20%).

There are simple and complex proteins of the nervous tissue.

The role of lipids in the structure of the shell

Lipids play a key role in the structure of the pulp membrane. They are the structural material of the nervous tissue and protect the axon from the loss of energy and ion currents. Lipid molecules have the ability to restore brain tissue after damage. Myelin lipids are responsible for the adaptation of the mature nervous system. They act as hormone receptors and communicate between cells.

The role of proteins

Of no small importance in the structure of the myelin layer are protein molecules. They, along with lipids, act as a building material of the nervous tissue. Their main task is to transport nutrients to the axon. They also decipher the signals entering the nerve cell and speed up the reactions in it. Participation in metabolism is an important function of myelin sheath protein molecules.

Myelination defects

Destruction of the myelin layer of the nervous system is a very serious pathology, due to which there is a violation of the transmission of the nerve impulse. She calls dangerous diseases often incompatible with life. There are two types of factors that influence the occurrence of demyelination:

• genetic predisposition to the destruction of myelin;
• influence on myelin of internal or external factors.
• Demyelization is divided into three types:
• acute;
• remitting;
• acute monophasic.

Why destruction occurs

Most common causes destruction of the pulpy membrane are:

• rheumatic diseases;
• a significant predominance of proteins and fats in the diet;
• genetic predisposition;
• bacterial infections;
• heavy metal poisoning;
• tumors and metastases;
• prolonged severe stress;
• bad ecology;
• pathology of the immune system;
• long-term use of neuroleptics.

Diseases due to demyelination

Demyelinating diseases of the central nervous system:

1. Canavan disease – genetic disease arising in early age. It is characterized by blindness, problems with swallowing and eating, impaired motor skills and development. Epilepsy, macrocephaly and muscular hypotension are also a consequence of this disease.
2. Binswanger's disease. Most often caused arterial hypertension. Patients expect thinking disorders, dementia, as well as violations of walking and the functions of the pelvic organs.
3. . May cause damage to several parts of the CNS. He is accompanied by paresis, paralysis, convulsions and impaired motor skills. Also, as symptoms of multiple sclerosis are behavioral disorders, weakening of the facial muscles and vocal cords, impaired sensitivity. Vision is disturbed, the perception of color and brightness changes. Multiple sclerosis is also characterized by disorders of the pelvic organs and degeneration of the brainstem, cerebellum, and cranial nerves.
4. Devic's disease- demyelination in optic nerve and spinal cord. The disease is characterized by impaired coordination, sensitivity and functions of the pelvic organs. It is distinguished by severe visual impairment and even blindness. AT clinical picture paresis, muscle weakness and autonomic dysfunction are also observed.
5. Osmotic demyelination syndrome. It occurs due to a lack of sodium in the cells. Symptoms are convulsions, personality disorders, loss of consciousness up to coma and death. The consequence of the disease are cerebral edema, hypothalamic infarction and hernia of the brain stem.
6. Myelopathy- various dystrophic changes in the spinal cord. They are characterized by muscle disorders, sensory disturbances, and pelvic organ dysfunction.
7. Leukoencephalopathy- destruction of the myelin sheath in the subcortex of the brain. Patients suffer from constant headache and epileptic seizures. There are also visual, speech, coordination, and walking impairments. Sensitivity decreases, personality and consciousness disorders are observed, dementia progresses.
8. Leukodystrophy- a genetic metabolic disorder that causes the destruction of myelin. The course of the disease is accompanied by muscle and movement disorders, paralysis, impaired vision and hearing, and progressive dementia.

Demyelinating diseases of the peripheral nervous system:

1. Guillain-Barré syndrome is an acute inflammatory demyelination. It is characterized by muscle and movement disorders, respiratory failure, partial or total absence tendon reflexes. Patients suffer from heart disease, impaired work digestive system and pelvic organs. Paresis and sensory disturbances are also signs of this syndrome.
2. Neural amyotrophy Charcot-Marie-Tooth - hereditary pathology myelin sheath. It is distinguished by sensory disturbances, limb dystrophy, spinal deformity and tremor.

This is only a part of the diseases that occur due to the destruction of the myelin layer. The symptoms are the same in most cases. An accurate diagnosis can only be made after computed or magnetic resonance imaging. An important role in the diagnosis is played by the level of qualification of the doctor.

Principles of Treatment of Shell Defects

Diseases associated with the destruction of the pulpy membrane are very difficult to treat. Therapy is aimed mainly at stopping the symptoms and stopping the destruction processes. The earlier the disease is diagnosed, the more likely it is to stop its course.

Myelin Repair Options

Thanks to timely treatment you can start the process of myelin repair. However, the new myelin sheath will not perform as well. In addition, the disease can become chronic stage, and the symptoms persist, only slightly smoothed out. But even a slight remyelination can stop the course of the disease and partially restore lost functions.

Modern drugs aimed at regenerating myelin are more effective, but they are very expensive.

Therapy

The following drugs and procedures are used to treat diseases caused by the destruction of the myelin sheath:

• beta-interferons (stop the course of the disease, reduce the risk of relapse and disability);
• immunomodulators (affect the activity of the immune system);
• muscle relaxants (contribute to the restoration of motor functions);

• nootropics (restore conductive activity);
• anti-inflammatory (relieve inflammatory process that caused the destruction of myelin);
• (prevent damage to brain neurons);
• painkillers and anticonvulsants;
• vitamins and antidepressants;
• CSF filtration (a procedure aimed at cleansing the cerebrospinal fluid).

Disease prognosis

Currently, the treatment of demyelination does not give a 100% result, but scientists are actively developing medicines aimed at restoring the pulpy membrane. Research is carried out in the following areas:

1. Stimulation of oligodendrocytes. These are the cells that make myelin. In an organism affected by demyelination, they do not work. Artificial stimulation of these cells will help start the process of repairing the damaged areas of the myelin sheath.
2. stem cell stimulation. Stem cells can turn into full-fledged tissue. There is a possibility that they can fill the fleshy shell.
3. Regeneration of the blood-brain barrier. During demyelination, this barrier is destroyed and allows lymphocytes to negatively affect myelin. Its restoration protects the myelin layer from attack by the immune system.

Perhaps soon, diseases associated with the destruction of myelin will no longer be incurable.

The myelin sheath of nerves is 70-75% lipids and 25-30% proteins. The composition of its cells also includes lecithin, a representative of phospholipids, whose role is very large: it takes part in many biochemical processes, improves the body's resistance to toxins, and lowers cholesterol levels.

The use of products containing lecithin is a good prevention and one of the ways to treat diseases associated with impaired activity of the nervous system. This substance is part of many cereals, soy, fish, egg yolk, brewer's yeast. Lecithin also contains: liver, olives, chocolate, raisins, seeds, nuts, caviar, dairy and dairy products. An additional source of this substance can be biologically active food additives.

You can restore the myelin sheath of nerves by including foods containing the amino acid choline in your diet: eggs, legumes, beef, nuts. Omega-3 polyunsaturated fatty acids are very useful. They are found in fatty fish, seafood, seeds, nuts, linseed oil and flaxseed. Omega-3 fatty acids can be sourced from: fish fat, avocado, walnuts, beans.

The composition of the myelin sheath includes vitamins B1 and B12, so it will be useful for the nervous system to include in the diet Rye bread, whole grains, dairy products, pork, fresh herbs. It is very important to consume enough folic acid. Its sources: legumes (peas, beans, lentils), citrus fruits, nuts and seeds, asparagus, celery, broccoli, beets, carrots, pumpkin.

Restoration of the myelin sheath of nerves contributes to copper. It contains: sesame seeds, pumpkin seeds, almonds, dark chocolate, cocoa, pork liver, seafood. For the health of the nervous system, it is necessary to include foods containing inositol in the diet: vegetables, nuts, bananas.

It is very important to support the immune system. If there are sources in the body chronic inflammation or autoimmune diseases disrupt the integrity of the nerves. In these cases, in addition to the main therapy, food and herbal anti-inflammatory drugs should be introduced into the menu: green tea, infusions of rosehip, nettle, yarrow, as well as foods rich in vitamins C and D. Vitamin C is found in large quantities in citrus fruits, berries, kiwi, cabbage, sweet peppers, tomatoes, spinach. Sources of vitamin D are eggs, dairy products, butter, seafood, fatty fish, cod liver and other fish.

A diet to restore the myelin sheath of nerves should contain sufficient amounts of calcium. It is part of many products: milk, cheese, nuts, fish, vegetables, fruits, cereals. For the full absorption of calcium, it is necessary to include magnesium (found in nuts, wholemeal bread) and phosphorus (found in fish) in the diet.

NERVE FIBERS

Nerve fibers are processes of neurons covered with glial sheaths. There are two types of nerve fibers - unmyelinated and myelinated. Both types consist of a centrally lying process of a neuron (an axial cylinder) surrounded by a sheath of oligodendroglia cells (in the PNS they are called lemmocytes or Schwann cells).

unmyelinated nerve fibers in an adult, they are located mainly in the autonomic nervous system and are characterized by a relatively low speed of nerve impulse conduction (0.5-2 m/s). They are formed by immersing the axial cylinder (axon) into the cytoplasm of lemmocytes, which are located in the form of strands. In this case, the plasmolemma of the lemmocyte bends, surrounding the axon, and forms a duplication - the mesaxon (Fig. 14-7). Often in the cytoplasm of one lemmocyte there can be up to 10-20 axle cylinders. Such a fiber resembles an electrical cable and is therefore called a cable-type fiber. The surface of the fiber is covered with a basement membrane. In the CNS, especially in the course of its development, unmyelinated fibers are described, consisting of a "naked" axon, devoid of a sheath of lemmocytes.

Rice. 14-7. Formation of myelinated (1-3) and unmyelinated (4) nerve fibers in the peripheral nervous system. The nerve fiber is formed by immersing the axon (A) of the nerve cell into the cytoplasm of the lemmocyte (LC). When a myelin fiber is formed, a duplication of the LC plasmolemma - mesaxon (MA) - is wound around A, forming turns of the myelin sheath (MO). In the myelin-free fiber shown in the figure, several A are immersed in the cytoplasm of the LC (cable-type fiber). I am the core of the LC.

myelinated nerve fibers found in the CNS and PNS and are characterized by a high speed of nerve impulse conduction (5-120 m/s). Myelinated fibers are usually thicker than unmyelinated ones and contain larger diameter axial cylinders. In the myelin fiber, the axial cylinder is directly surrounded by a special myelin sheath, around which there is a thin layer that includes the cytoplasm and the nucleus of the lemmocyte - the neurolemma (Fig. 14-8 and 14-9). Outside, the fiber is also covered with a basement membrane. The myelin sheath contains high concentrations of lipids and is intensely stained with osmic acid, having the appearance of a homogeneous layer under a light microscope, but under an electron microscope it is found that it arises as a result of the fusion of numerous (up to 300) membrane coils (plates).

Rice. 14-8. The structure of the myelinated nerve fiber. Myelin fiber consists of an axial cylinder, or axon (A), directly surrounded by a myelin sheath (MO) and a neurolemma (NL), including the cytoplasm (CL) and lemmocyte nucleus (NL). Outside, the fiber is covered with a basement membrane (BM). The areas of the MO, in which the gaps between the myelin turns are preserved, filled with CL and therefore not stained with osmium, have the form of myelin notches (MN).

Myelin sheath formation occurs during the interaction of the axial cylinder and oligodendroglia cells with some differences in the PNS and CNS.

Myelin sheath formation in the PNS : the immersion of the axial cylinder into the lemmocyte is accompanied by the formation of a long mesaxon, which begins to rotate around the axon, forming the first loosely arranged turns of the myelin sheath (see Fig. 14-7). As the number of turns (plates) increases in the process of myelin maturation, they are arranged more and more densely and partially merge; the gaps between them, filled with the cytoplasm of the lemmocyte, are preserved only in separate areas that are not stained with osmium - myelin notches (Schmidt-Lanterman). During the formation of the myelin sheath, the cytoplasm and the nucleus of the lemmocyte are pushed to the periphery of the fiber, forming the neurolemma. The myelin sheath has a discontinuous course along the length of the fiber.

Rice. 14-9. Ultrastructural organization of the myelinated nerve fiber. Around the axon (A) there are coils of the myelin sheath (MMO), externally covered with a neurolemma, and which includes the cytoplasm (CL) and the nucleus of the lemmocyte (NL). The fiber is surrounded on the outside by a basement membrane (BM). CL, in addition to the neurolemma, forms an inner sheet (IL) directly adjacent to A (located between it and the SMO), it is also contained in the zone corresponding to the border of neighboring lemmocytes - the nodal intercept (NC), where the myelin sheath is absent, and in areas of loose WMO stacking - myelin notches (MN).

Nodal interceptions (Ranvier)- areas in the region of the border of neighboring lemmocytes, in which the myelin sheath is absent, and the axon is covered only by interdigitating processes of neighboring lemmocytes (see Fig. 14-9). Nodal interceptions are repeated along the course of the myelin fiber with an interval equal, on average, to 1-2 mm. In the region of the nodal node, the axon often expands, and its plasmolemma contains numerous sodium channels (which are absent outside the nodes under the myelin sheath).

Propagation of depolarization in myelin fiber carried out in jumps from interception to interception (saltatory). Depolarization in the region of one nodal junction is accompanied by its rapid passive propagation along the axon to the next junction (since current leakage in the internodal region is minimal due to the high insulating properties of myelin). In the area of ​​the next intercept, the impulse causes the existing ion channels to turn on and a new area of ​​local depolarization appears, etc.

Myelin sheath formation in the CNS: the axial cylinder does not sink into the cytoplasm of the oligodendrocyte, but is covered by its flat process, which subsequently rotates around it, losing the cytoplasm, and its coils turn into plates of the myelin sheath

elbows (Fig. 14-10). In contrast to Schwann cells, one CNS oligodendrocyte with its processes can participate in the myelination of many (up to 40-50) nerve fibers. The axon sites in the area of ​​nodes of Ranvier in the CNS are not covered by the cytoplasm of oligodendrocytes.

Rice. 14-10. The formation of myelin fibers by oligodendrocytes in the CNS. 1 - the axon (A) of the neuron is covered by a flat process (PO) of the oligodendrocyte (ODC), the coils of which turn into plates of the myelin sheath (MO). 2 - one ODC with its processes can participate in the myelination of many A. Areas A in the area of ​​nodal intercepts (NC) are not covered by the cytoplasm of ODC.

Violation of the formation and damage of formed myelin underlie a number of serious diseases of the nervous system. Myelin in the CNS may be a target for autoimmune damage T-lymphocytes and macrophages with its destruction (demyelinization). This process is active in multiple sclerosis - serious illness unclear (probably viral) nature, associated with a disorder of various functions, the development of paralysis, loss of sensitivity. Character neurological disorders determined by the topography and size of damaged areas. With some metabolic disorders, there are disorders in the formation of myelin - leukodystrophy, manifested in childhood by severe lesions of the nervous system.

Classification of nerve fibers

Classification of nerve fibers is based on differences in their structure and function (velocity of nerve impulses). There are three main types of nerve fibers:

1. Type A fibers - thick, myelinated, with far-distant nodal intercepts. Conduct impulses at high speed

(15-120 m/s); subdivided into 4 subtypes (α, β, γ, δ) with decreasing diameter and speed of impulse conduction.

2. Type B fibers - medium thickness, myelin, smaller diameter,

than type A fibers, with a thinner myelin sheath and a lower speed of nerve impulse conduction (5-15 m/s).

3. Type C fibers - thin, unmyelinated, conduct impulses at a relatively low speed(0.5-2 m/s).

Regeneration of nerve fibers in the PNS includes a naturally unfolding complex sequence of processes during which the neuron process actively interacts with glial cells. The actual regeneration of the fibers follows a series of reactive changes caused by their damage.

Reactive changes in the nerve fiber after its transection. During the 1st week after cutting the nerve fiber, ascending degeneration of the proximal (closest to the body of the neuron) part of the axon develops, at the end of which an extension (retraction flask) is formed. The myelin sheath in the area of ​​damage disintegrates, the body of the neuron swells, the nucleus shifts to the periphery, the chromatophilic substance dissolves (Fig. 14-11).

In the distal part of the fiber, after its transection, descending degeneration is noted with complete destruction of the axon, the breakdown of myelin, and subsequent phagocytosis of detritus by macrophages and glia.

Structural transformations during the regeneration of the nerve fiber. After 4-6 weeks. the structure and function of the neuron are restored, thin branches (growth cones) begin to grow from the retraction flask in the direction of the distal part of the fiber. Schwann cells in the proximal part of the fiber proliferate, forming ribbons (Büngner) parallel to the course of the fiber. In the distal part of the fiber, Schwann cells also persist and mitotically divide, forming ribbons that connect with similar formations in the proximal part.

The regenerating axon grows in the distal direction at a rate of 3-4 mm/day. along the Büngner tapes, which play a supporting and guiding role; Schwann cells form a new myelin sheath. Collaterals and axon terminals are restored within a few months.

Rice. 14-11. Regeneration of the myelinated nerve fiber (according to R.Krstic, 1985, with changes). 1 - after transection of the nerve fiber, the proximal part of the axon (A) undergoes ascending degeneration, the myelin sheath (MO) in the area of ​​damage disintegrates, the perikaryon (PC) of the neuron swells, the nucleus shifts to the periphery, the chromatophilic substance (CS) disintegrates (2). The distal part associated with the innervated organ (in the given example, the skeletal muscle) undergoes downward degeneration with complete destruction of A, disintegration of MO and phagocytosis of detritus by macrophages (MF) and glia. Lemmocytes (LC) persist and mitotically divide, forming strands - Büngner's ribbons (LB), connecting with similar formations in the proximal part of the fiber (thin arrows). After 4-6 weeks, the structure and function of the neuron are restored, thin branches grow distally from the proximal part A (bold arrow), growing along the LB (3). As a result of regeneration of the nerve fiber, the connection with the target organ (muscle) is restored and its atrophy caused by impaired innervation regresses (4). In the event of an obstruction (P) on the path of regenerating A (for example, a connective tissue scar), the components of the nerve fiber

form a traumatic neuroma (TN), which consists of growing branches A and LC (5).

regeneration conditions are: no damage to the body of the neuron, a small distance between the parts of the nerve fiber, the absence of connective tissue that can fill the gap between the parts of the fiber. When an obstruction occurs on the path of the regenerating axon, a traumatic (amputation) neuroma is formed, which consists of a proliferating axon and Schwann cells that are soldered into the connective tissue.

There is no regeneration of nerve fibers in the CNS : although CNS neurons have the ability to restore their processes, this does not happen, apparently due to the adverse influence of the microenvironment. After damage to a neuron, microglia, astrocytes, and hematogenous macrophages phagocytize detritus in the area of ​​the destroyed fiber, and proliferating astrocytes form a dense glial scar in its place.

NERVE ENDINGS

Nerve endings- terminal devices of nerve fibers. According to their function, they are divided into three groups:

1) interneuronal contacts (synapses)- provide a functional connection between neurons;

2) efferent (effector) endings- transmit signals from the nervous system to the executive organs (muscles, glands), are present on axons;

3) receptor (sensitive) endingsperceive irritations from the external and internal environment, are present on the dendrites.

INTERNEURONAL CONTACTS (SYNAPSE)

Interneuronal contacts (synapses) divided into electrical and chemical.

electrical synapses rare in the CNS of mammals; they have the structure of gap junctions, in which the membranes of synaptically connected cells (pre- and postsynaptic) are separated by a 2-nm-wide gap pierced by connexons. The latter are tubes formed by protein molecules and serve as water channels through which small molecules and ions can be transported from one cell to another.

another (see chapter 3). When an action potential propagating across the membrane of one cell reaches the gap junction, an electrical current passively flows through the gap from one cell to another. The impulse is capable of being transmitted in both directions and with virtually no delay.

Chemical synapses- the most common type in mammals. Their action is based on the conversion of an electrical signal into a chemical signal, which is then converted back into an electrical signal. The chemical synapse consists of three components: the presynaptic part, the postsynaptic part, and the synaptic cleft (Fig. 14-12). The presynaptic part contains a (neuro)transmitter, which, under the influence of a nerve impulse, is released into the synaptic cleft and, binding to receptors in the postsynaptic part, causes changes in the ion permeability of its membrane, which leads to its depolarization (in excitatory synapses) or hyperpolarization (in inhibitory synapses). ). Chemical synapses differ from electrical synapses in one-way conduction of impulses, a delay in their transmission (a synaptic delay of 0.2–0.5 ms), and the provision of both excitation and inhibition of the postsynaptic neuron.

Rice. 14-12. The structure of a chemical synapse. The presynaptic part (PRSP) has the form of a terminal button (CB) and includes: synaptic vesicles (SP), mitochondria (MTX), neurotubules (NT), neurofilaments (NF), presynaptic membrane (PRSM) with presynaptic compaction (PRSU). The postsynaptic part (PSCH) includes the postsynaptic membrane (POSM) with the postsynaptic compaction (POSU). The synaptic cleft (SC) contains intrasynaptic filaments (ISF).

1. presynaptic part is formed by the axon along its course (passing synapse) or is an extended end part of the axon (terminal bud). It contains mitochondria, aER, neurofilaments, neurotubules and synaptic vesicles with a diameter of 20-65 nm, which contain the neurotransmitter. The shape and nature of the contents of the vesicles depend on the neurotransmitters in them. Round light vesicles usually contain acetylcholine, vesicles with a compact dense center - norepinephrine, large dense vesicles with a light submembrane rim - peptides. Neurotransmitters are produced in the body of the neuron and are transported to the axon endings by the mechanism of rapid transport, where they are deposited. Partially, synaptic vesicles are formed in the synapse itself by splitting off from the cisterns of the aER. On the inside The plasmalemma facing the synaptic cleft (presynaptic membrane) has a presynaptic seal formed by a fibrillar hexagonal protein network, the cells of which contribute to a uniform distribution of synaptic vesicles over the surface of the membrane.

2. postsynaptic part It is represented by a postsynaptic membrane containing special complexes of integral proteins - synaptic receptors that bind to a neurotransmitter. The membrane is thickened due to the accumulation of dense filamentous protein material under it (postsynaptic compaction). Depending on whether the postsynaptic part of the interneuronal synapse is the dendrite, the body of the neuron, or (less often) its axon, synapses are divided into axo-dendritic, axosomatic and axo-axonal, respectively.

3. synaptic cleft 20-30 nm wide sometimes contains transverse glycoprotein intrasynaptic filaments 5 nm thick, which are elements of a specialized glycocalyx that provide adhesive bonds of the pre- and post-synatic parts, as well as directed diffusion of the mediator.

The mechanism of transmission of a nerve impulse in a chemical synapse. Under the influence of a nerve impulse, voltage-dependent calcium channels of the presynaptic membrane are activated; Sa 2+ rushes into the axon, the membranes of synaptic vesicles in the presence of Ca2+ merge with the presynaptic membrane, and their contents (mediator) are released into the synaptic cleft by the mechanism of exocytosis. By acting on the receptors of the postsynaptic membrane, the mediator causes either its depolarization, the emergence of a postsynaptic action potential and the formation of a nerve impulse, or its hyperpigmentation.

polarization, causing an inhibitory response. Excitatory mediators, for example, are acetylcholine and glutamate, while inhibition is mediated by GABA and glycine.

After the termination of the interaction of the mediator with the receptors of the postsynaptic membrane, most of its endocytosis is captured by the presynaptic part, the smaller part is scattered in space and captured by the surrounding glial cells. Some mediators (for example, acetylcholine) are broken down by enzymes into components that are then captured by the presynaptic part. Synaptic vesicle membranes embedded in the presynaptic membrane are further incorporated into endocytic lined vesicles and reused to form new synaptic vesicles.

In the absence of a nerve impulse, the presynaptic part releases individual small portions of the mediator, causing spontaneous miniature potentials in the postsynaptic membrane.

EFFERENT (EFFECTOR) NERVE ENDINGS

Efferent (effector) nerve endings Depending on the nature of the innervated organ, they are divided into motor and secretory. Motor endings are found in striated and smooth muscles, secretory - in the glands.

Neuromuscular ending (neuromuscular junction, motor plaque) - the motor ending of the axon of the motor neuron on the fibers of the striated somatic muscles - consists of the terminal branching of the axon, which forms the presynaptic part, a specialized area on the muscle fiber, corresponding to the postsynaptic part, and the synaptic cleft separating them (Fig. 14-13).

In large muscles that develop significant strength, one axon, branching, innervates a large number of(hundreds and thousands) of muscle fibers. On the contrary, in small muscles that perform fine movements (for example, the external muscles of the eye), each fiber or a small group of them is innervated by a separate axon. One motor neuron, together with the muscle fibers innervated by it, forms a motor unit.

presynaptic part. Near the muscle fiber, the axon loses its myelin sheath and gives rise to several branches that