What is the myelin sheath and how does it function. How does myelination occur in the nervous system. Why is myelin crucial for efficient nerve signal transmission. What are the consequences of myelin damage. How do Schwann cells and oligodendrocytes contribute to myelination.

The Myelin Sheath: A Crucial Component of the Nervous System

The myelin sheath is a vital structure in the nervous system, playing a pivotal role in the efficient transmission of nerve signals. This protective layer, composed of lipids and proteins, wraps around the axons of neurons in both the central nervous system (CNS) and peripheral nervous system (PNS). Understanding the myelin sheath’s structure, function, and formation is essential for comprehending how our nervous system operates and why certain neurological conditions occur.

Discovery and Composition of Myelin

The discovery of myelin dates back to the mid-19th century when German pathologist Rudolf Virchow observed a glistening white substance surrounding axons under a microscope. He coined the term ‘myelin’ from the Greek word ‘myelós’, meaning core. Initially believed to be at the core of the axon, it was later determined that myelin actually wraps around the axons of neurons.

Myelin is composed of:

• Lipids
• Proteins

These components form a fatty substance with a white appearance, creating the protective sleeve that envelops the axon. The myelin sheath consists of multiple concentric layers of plasma membrane tightly wound around the axon.

The Crucial Functions of Myelin Sheath

The myelin sheath serves several essential functions in the nervous system, primarily centered around enhancing the speed and efficiency of nerve signal transmission.

Insulation and Signal Propagation

How does the myelin sheath facilitate faster nerve signal transmission? The myelin sheath acts as an insulator for axons, similar to the insulation on electrical wires. As a low electrical condenser with high electrical resistance, it insulates without disrupting the electrical signals traveling along the axon. This insulation allows axons to conduct electrical signals at much higher speeds compared to unmyelinated axons.

The degree of myelination directly correlates with the speed of electrical transmission. Heavily myelinated axons can conduct impulses at speeds of approximately 70 to 120 meters per second – comparable to the speed of a race car.

Prevention of Signal Leakage

Another crucial function of the myelin sheath is preventing electrical impulses from escaping the axon. It blocks the movement of ions into or out of the neuron, a process known as depolarization. This ensures that the current of action potential flows only down the axon, facilitating efficient and directed signal transmission.

Nodes of Ranvier and Saltatory Conduction

While the myelin sheath covers most of the axon, it features small, uncovered gaps called nodes of Ranvier. These specialized molecular structures contain clusters of voltage-sensitive sodium and potassium ion channels. As electrical impulses cannot travel through the myelin sheath, they “jump” from one node to another in a process called saltatory conduction.

Why is saltatory conduction important? This type of conduction allows for rapid formation of electrical impulses and requires less energy compared to signal transmission in unmyelinated axons. The energy efficiency of myelinated axons is a key advantage in the nervous system’s overall function.

The Process of Myelination: How Myelin Sheaths Form

Myelination refers to the formation of the myelin sheath around axons. This process is crucial for the development and function of the nervous system.

Myelinated vs. Unmyelinated Axons

Axons surrounded by a myelin sheath are termed myelinated axons, while those without this insulating layer are called unmyelinated axons. The presence of myelin significantly impacts an individual’s response time to stimuli. More myelinated axons result in quicker responses due to the increased speed of nerve impulse conduction.

In contrast, unmyelinated axons conduct signals more slowly as the electrical impulse must travel through each part of the cell without the benefit of saltatory conduction.

Glial Cells: The Myelin Producers

Myelin sheath production is carried out by specialized glial cells. These cells, found in both the CNS and PNS, play a crucial role in maintaining homeostasis and providing support and protection for neurons.

Two types of glial cells are responsible for myelin production:

1. Schwann cells (in the PNS)
2. Oligodendrocytes (in the CNS)

Schwann Cells: Myelination in the Peripheral Nervous System

Schwann cells are the primary myelinating cells in the peripheral nervous system. These cells originate from the neural crest, a group of embryonic cells, and begin myelinating axons during fetal development.

Structure and Function of Schwann Cells

Schwann cells are surrounded by sheets of tissue known as basal lamina. The outer surface of the Schwann cell forms the outermost layer of the myelin sheath, while the inner surface wraps around the axon multiple times, creating the characteristic multi-layered structure of myelin.

How do Schwann cells myelinate axons? The process begins with a Schwann cell attaching to an axon and extending its plasma membrane. As it rotates around the axon, it forms multiple layers of myelin. Each Schwann cell typically myelinates a single segment of one axon, with adjacent Schwann cells covering consecutive segments along the axon’s length.

Role in Nerve Regeneration

Schwann cells play a crucial role in nerve regeneration following injury in the PNS. When an axon is damaged, Schwann cells can dedifferentiate and proliferate, forming a guide for the regenerating axon. This process, known as Wallerian degeneration, is a key factor in the PNS’s ability to recover from injury more effectively than the CNS.

Oligodendrocytes: Myelination in the Central Nervous System

Oligodendrocytes are the myelin-producing cells of the central nervous system, including the brain and spinal cord. These cells differ from Schwann cells in several important ways.

Structure and Function of Oligodendrocytes

Unlike Schwann cells, oligodendrocytes can myelinate multiple axon segments simultaneously. A single oligodendrocyte can extend numerous processes, each of which can wrap around and myelinate a different axon segment. This ability allows for more efficient myelination in the densely packed environment of the CNS.

How do oligodendrocytes form myelin sheaths? The process begins with the oligodendrocyte extending a process that wraps around an axon segment. As the process rotates around the axon, it forms multiple layers of myelin, similar to the action of Schwann cells in the PNS.

Challenges in CNS Regeneration

Why is regeneration more challenging in the CNS compared to the PNS? Unlike Schwann cells, oligodendrocytes do not dedifferentiate and proliferate following injury. This limitation, combined with the presence of growth-inhibiting factors in the CNS environment, makes regeneration and remyelination in the CNS more difficult. This is one reason why conditions affecting the CNS, such as multiple sclerosis, can have such devastating effects.

The Impact of Myelin Damage on Neurological Function

Damage to the myelin sheath can have severe consequences for neurological function. Several conditions are associated with myelin destruction or dysfunction.

Multiple Sclerosis: A Prime Example of Demyelination

Multiple sclerosis (MS) is perhaps the most well-known condition associated with myelin damage. In MS, the immune system mistakenly attacks and destroys myelin in the CNS. This demyelination disrupts nerve signal transmission, leading to a wide range of neurological symptoms.

What are the common symptoms of multiple sclerosis? Symptoms can vary widely but often include:

• Fatigue
• Vision problems
• Numbness and tingling
• Muscle weakness
• Balance and coordination issues
• Cognitive changes

Other Conditions Affecting Myelin

Several other conditions can affect myelin integrity:

1. Guillain-Barré syndrome: An autoimmune disorder affecting myelin in the PNS
2. Charcot-Marie-Tooth disease: A group of inherited disorders affecting PNS myelin
3. Leukodystrophies: A group of rare genetic disorders characterized by progressive degeneration of white matter in the brain

In each of these conditions, damage to or dysfunction of myelin leads to impaired nerve signal transmission, resulting in various neurological symptoms.

Myelin Repair and Regeneration: Prospects for Treatment

Given the critical role of myelin in nervous system function, research into myelin repair and regeneration is a key area of focus in neuroscience and medicine.

Natural Remyelination Processes

The nervous system does have some capacity for natural remyelination, particularly in the PNS. Schwann cells can dedifferentiate and proliferate following injury, supporting axon regeneration and remyelination. In the CNS, oligodendrocyte precursor cells can differentiate into new oligodendrocytes to remyelinate damaged axons, although this process is less efficient than in the PNS.

Therapeutic Approaches to Promoting Remyelination

What strategies are researchers exploring to enhance myelin repair? Several approaches are under investigation:

• Stem cell therapies: Using stem cells to generate new myelin-producing cells
• Pharmacological interventions: Developing drugs that promote remyelination or protect existing myelin
• Gene therapies: Targeting genes involved in myelin production and maintenance
• Immunomodulation: Regulating the immune system to prevent myelin damage in autoimmune conditions

These approaches hold promise for treating conditions characterized by myelin damage, potentially slowing or even reversing the progression of diseases like multiple sclerosis.

The Future of Myelin Research: Emerging Trends and Possibilities

As our understanding of myelin biology continues to grow, new avenues for research and potential therapies are emerging.

Advanced Imaging Techniques

How are researchers gaining new insights into myelin structure and function? Advanced imaging techniques, such as high-resolution MRI and two-photon microscopy, are allowing scientists to visualize myelin in unprecedented detail. These tools are providing new insights into myelin formation, maintenance, and repair in both healthy and diseased states.

The Role of Myelin in Neuroplasticity

Recent research has highlighted the dynamic nature of myelin, suggesting that changes in myelination may play a role in learning and memory. This concept of “myelin plasticity” opens up new possibilities for understanding brain function and potentially enhancing cognitive abilities.

Myelin and Neurodegenerative Diseases

While traditionally associated with conditions like multiple sclerosis, myelin dysfunction is increasingly recognized as a factor in other neurodegenerative diseases. How might myelin play a role in conditions like Alzheimer’s or Parkinson’s disease? Researchers are exploring the potential connections between myelin health and these widespread neurological disorders.

As research in these areas progresses, our understanding of myelin’s role in nervous system function continues to expand. This knowledge not only deepens our comprehension of neurological processes but also paves the way for novel therapeutic approaches to a wide range of neurological conditions.

What They Are, Their Function, & Damage

Myelin sheath is a substance that is found on neurons within the central nervous system (CNS) and the peripheral nervous system (PNS).

Myelin sheath is the protective layer that wraps around the axons of neurons to aid in insulating the neurons, and to increase the number of electrical signals being transferred.

An axon is usually wrapped by the myelin sheath around its whole length in order to increase the speed of these electrical signals, allowing all actions to be conducted quickly.

Myelin sheath consists of lipids and proteins which make up a fatty substance and is white in appearance. This forms the protective sleeve that wraps around the axon of neurons. The sheath is made up of many concentric layers of plasma membrane, wrapped tightly around the axon.

There are breaks of between 0.2 and 2 mm. in the myelin sheath, these are called nodes of Ranvier. Action potentials (nerve impulses) traveling down the axon “jump” from node to node. This speeds up the transmission.

Myelin was discovered in the mid-19th century when scientists were observing neurons through a microscope, and they noticed a glistening white substance surrounding the axons. Rudolf Virchow, a German pathologist who made this observation, coined the term ‘myelin’ from the Greek word myelós, which means core.

At the time, it was believed that the myelin was at the core of the axon. However, it was later found to be a substance which wraps around the axons of neurons.

Table of Contents

Functions

Myelin sheath’s primary function is to provide insulation to the axons of the neuron it surrounds. This insulation protects these axons in the same way that electrical wires have insulation.

Myelin sheath is a low electrical condenser with high electrical resistance, which means it can act as an insulator without disrupting the electrical signals traveling down the axon.

Since myelin sheath provides insulation to axons, this allows these axons to conduct electrical signals at a higher speed than if they were not insulated by myelin. Thus, the more thoroughly myelinated an axon is, the higher the speed of electrical transmission.

One of the most myelinated axons, for instance, can conduct impulses at a speed of approximately 70 to 120 m/s, the speed of a race car. Similarly, the myelin sheath around an axon can prevent electrical impulses from traveling through the sheath and out of the axon.

It prevents the movement of ions into or out of the neuron, also known as depolarization. This means the current of action potential will only flow down the axon. The more action potential, the more neurons can communicate with each other, transfer electrical and chemical messages, and keep the brain healthy and functioning properly.

Whilst the myelin sheath wraps around the axons, there are some small, uncovered gaps between the myelin sheath, called the nodes of Ranvier. These are specialized molecular structures created by the myelin sheath, which contains clusters of voltage-sensitive sodium and potassium ion channels.

As the electrical impulses cannot travel through the myelin sheath, it instead ‘jumps’ from one node of Ranvier to another in a type of conduction called saltatory conduction.

This type of conduction is important for electrical impulses to be formed quickly and means that less energy is required for the conduction of electrical signals. This is because less energy is needed in myelinated axons to conduct impulses.

Myelination

Myelination is the formation of a myelin sheath. Therefore, axons covered by this insulating sleeve of protection are said to be myelinated axons. If an axon is not surrounded by a myelin sheath, it is said to be unmyelinated.

The more myelinated axons someone has, the quicker their responses to stimuli will be due to myelin sheaths increasing the conduction of nerve impulses. Consequently, unmyelinated axons will mean an individual will not respond quickly.

Likewise, in unmyelinated axons, the electrical signal will not be sped up by the nodes of Ranvier, meaning the signals will travel through each part of the cell, which slows down the speed of the signal’s conduction.

Myelin sheath is produced by different types of glia cells. Glia cells are located in the CNS and PNS, which work to maintain homeostasis, and provide support and protection for neurons.

The two types of glia cells that produce myelin are Schwann cells and oligodendrocytes. Schwann cells are located within the peripheral nervous system (PNS) whereas oligodendrocytes are located within the central nervous system (CNS).

Schwann cells

Schwann cells originate from the neural crest, which is a group of embryonic cells. As such, Schwann cells will first start to myelinate axons during foetal development. Schwann cells are surrounded by sheets of tissue known as basal lamina.

The outside of the basal lamina is covered in a layer of connective tissues known as the endoneurium. The endoneurium contains blood vessels, macrophages, and fibroblasts. Finally, the inner surface area of the lamina layer faces the plasma membrane of the Schwann cells.

For the myelin sheath to be created by Schwann cells in the PNS, the plasma membrane of these cells needs to wrap itself around the axons of the neuron concentrically, spiralling to add membrane layers.

This plasma membrane contains high levels of fat which is essential for the construction of myelin sheath. Sometimes, as many as 100 revolutions of Schwann cell spiral around the axons of the neurons.

Oligodendrocytes

Within the CNS, oligodendrocytes are the glia cells that also create myelin sheaths. Oligodendrocytes are star-shaped cells that have about 15 arms coming out of their cell body, meaning it is able to myelinate multiple axons at one time.

In a similar fashion to Schwann cells, oligodendrocytes spiral around the axons of neurons to form a myelin sheath. The cell body and the nucleus of the oligodendrocytes, however, remain separate from the sheath and so do not wrap around the axon, unlike Schwann cells.

The oligodendrocytes repeatedly spiral around the axon to form a lipid-rich membrane, thus functioning similarly to Schwann cells.
One oligodendrocyte can myelinate multiple axons at once in a coordinated process and simultaneously.

The onset of myelination is often triggered by neuronal activity in the CNS. This was proven in studies of rats, some of which were grown in the dark and some in the light.

It was found that the optic nerves of the rate of rats who grew up in the dark had fewer developed myelinated axons than those who did not grow up in the dark.

Overall, it has been found that the degree of myelination depends on the amount of neuronal activity, with increased neuronal activity increasing the amount of myelination.

Does Myelination Occur Throughout Life?

Myelination occurs during embryonic development and is then a continuous process from birth, maturing at about 2 years of age. Once at this stage, motor and sensory systems are matured, and cerebral myelination is mostly complete.

However, some processes are myelinated later in life, with some connections between the thalamus and prefrontal cortex maturing between the ages of 5 and 7 years of age.

Similarly, myelination of connections between association areas of the cerebral cortex continues into the 20s and 30s of individuals. Typically, myelination within the brainstem and cerebellum will mature first, followed by maturation of myelination in the lobes of the cerebral cortex.

Most individuals between the ages of 20 and 29 will be at their peak in their ability to perform physically due to myelination being matured in relevant areas.

However, myelination continues to develop throughout adulthood in regions responsible for integrating information for purposeful acti,vities such as in association areas, finally peaking at around 50.

Although there is continued myelination in association areas, the nervous system begins to decline in general from 20, with the thinning of the cortex and the number of oligodendrocytes decreasing.

Clinical Aspects

Issues with myelination could result from damage, infections, trauma, genetic mutations, and autoimmune diseases. If the myelin sheath on the axons is damaged or unable to be formed, this can result in electrical signals traveling down the axons being slower or disrupted.

The myelin sheath is crucial for the normal operation of the neurons within the nervous system: the loss of the insulation it provides can be detrimental to normal function.

Ultimately, this could impair the myelination process and the functions of the Schwann cells and oligodendrocytes, leading to neurodegeneration.

Depending on the extent of the issue and the condition experienced, an individual with myelination problems may be experiencing one or more of the following symptoms:

• Numbness
• Dizziness
• Uncoordinated or clumsy movements
• Loss of reflexes
• Muscle weakness
• Muscle spasms
• Blurred vision or vision loss
• Sensory changes or sensory loss
• Pain
• Muscle stiffness

The process of myelin being destroyed or not functioning properly is called demyelination. Diseases associated with demyelination can range from acute to chronic.

A condition called Guillain-Barre Syndrome is a rare autoimmune disease that damages the healthy neurons of the PNS.

This can result in weakness and numbness and may eventually cause paralysis, making it a life-threatening condition. As this condition causes damage to the axons of neurons, it can lead to electrical conduction being blocked.

Multiple sclerosis (MS) is another demyelinating condition that affects the myelin sheath. This disease causes the immune system of individuals to attack the CNS, meaning the myelin sheath will be damaged.

MS can weaken muscles, damage coordination, and can cause paralysis in the worst conditions. With MS, the body’s immune system will treat myelin as a threat and will attack the myelin as well as the cells that make it.

This condition, therefore, makes it difficult for electrical signals to be conducted through the neurons, resulting in compromised communication between neurons.

Finally, peripheral nerve tumors, such as Schwannomas are conditions that affect the Schwann cells that produce myelin sheath. A schwannoma is a tumor that is usually benign but, in rare instances, can be harmful and cancerous.

Although these are rarely harmful, they can result in nerve damage and a loss of motor control. These tumors affect the cells that produce myelin sheath in the PNS, this can negatively affect how the axons conduct electrical impulses, resulting in symptoms such as muscle weakness, numbness, and pain.

References

Cech, D. J., & Martin, S. T. (2011). Functional Movement Development Across the Life Span-E-Book . Elsevier Health Sciences.

Moore, S., Meschkat, M., Ruhwedel, T., Trevisiol, A., Tzvetanova, I. D., Battefeld, A., Kusch, K., Kole, M. H. P., Strenzke, N., Möbius, W., de Hoz, L. & Nave, K. A. (2020). A role of oligodendrocytes in information processing. Nature communications, 11 (1), 1-15.

Kirkwood, C. (2015, March 24). Myelin: An Overview . Brain Facts. https://www.brainfacts.org/brain-anatomy-and-function/anatomy/2015/myelin

Ratini, M. (2019, August 7). What Is a Myelin Sheath? WebMD. https://www.webmd.com/multiple-sclerosis/myelin-sheath-facts

Osika, A. (2020, October 29). The myelin sheath and myelination . Kenhub. https://www.kenhub.com/en/library/anatomy/the-myelin-sheath-and-myelination

Guy-Evans, O. (2021, Feb 15). Schwann cells . Simply Psychology. www.www.www.www.www.www.simplypsychology.org/schwann-cells.html

Nerve cells (neurons) | MS Trust

Last updated: 23 November 2022

Nerve cells carry messages between the central nervous system and the organs and limbs of the body.  In multiple sclerosis (MS), nerve cells or neurons are damaged by inflammation and demyelination can occur.

Multiple sclerosis is thought to be partly an autoimmune and partly a neurodegenerative condition. For some reason, the body’s immune system starts to mistakenly attack cells within the central nervous system. Initially the body can repair the damage to some extent, but with time nerve cells may begin to die. Scars develop on the damaged nerves. This scar tissue is what forms the lesions that show up as white regions on MRI scans.

Although other cells die and are replaced, many neurons are never replaced when they die. If you lose too many neurons, you may develop permanent disability. The disability you experience relates to the neurons which are damaged. For example, if you lose some of the neurons in your spine, your legs could be affected, leading to problems with walking.

How do neurons work?

Neurons have specialised extensions called dendrites and axons. A neuron usually has a number of dendrites but only one axon, although this axon may have extensive branching. The axon can be as long as one metre, making neurons some of the longest cells in the body.

Information enters the neuron via the dendrites, passes through the cell body and then along the axon until it reaches the synapse. The synapse is the space between an axon and a dendrite of another neuron.

To cross the synapse, neurotransmitters are released at the end of the neuron. They are collected by receptors on the dendrites of neighbouring neurons, and the message continues on its way.

The axon is surrounded by a sheath of fatty protein called myelin. Myelin acts as insulation to the axon and prevents messages becoming interrupted. The myelin sheath has short gaps about one micrometre apart known as Nodes of Ranvier. Nerve messages leap along the axon from node to node. The thickness of the myelin sheath and the size of the gap between nodes determine the speed of messages, which can be as fast as 120 metres/second (268mph).

Nerve cells are surrounded by support cells called glial cells. They include oligodendrocytes which produce myelin.

How does MS damage the nerve cells?

During an MS attack, the immune system triggers inflammation along the nerves and at the glial cells. Oligodendrocytes are damaged, and myelin is damaged and stripped away from the axon. This process is called demyelination. Messages that pass along a demyelinated nerve become delayed or blocked.

As the central nervous system controls processes throughout the body, a wide range of symptoms can occur, depending on where the nerve damage has happened. The range of symptoms is different for each person with MS.

Can nerve damage be repaired?

Once the inflammation caused by the immune attack is over, it is possible for the body to replace damaged myelin. This process is known as remyelination. Although the new myelin can work effectively, it tends to be thinner than unaffected myelin and so messages through the affected nerves may not be as fast as before the attack.

Remyelination tends to occur in the earlier stages of MS but, with repeated relapses or attacks, oligodendrocytes become damaged and destroyed. Eventually, they may not be able to produce more myelin. If an axon is left without the protection of myelin it will be more vulnerable to damage and may die.

Your central nervous system is able to overcome small areas of nerve damage by rerouting messages using undamaged nerve cells. This ability to adapt to avoid damaged areas is called plasticity. Messages may take longer to get through but your symptoms will improve to some extent.

Should the area of damage become too large, this rerouting process is no longer able to compensate. Messages to or from that part of the central nervous system are permanently blocked, resulting in symptoms that do not improve for you.

Remyelination and neuroprotection are potential areas where new treatments could be developed. Some research is looking into drugs that protect nerves from damage and so halt or slow down the progression of MS. Some research is investigating drugs that promote myelin repair, which would mean that damage could be reversed and function improved.

Find out more

Read more about what happens to the nervous system in MS in these other webpages in our A-Z.

• Glial cells
• Neuroprotection
• Central nervous system (CNS)

Any other questions?

We are here to support you. You may have MS yourself or be a friend or family member of someone with the condition.

Our experienced Helpline team are here to help you find all the information you need about multiple sclerosis. We’ll try to answer any question that you have about MS and if we can’t find the answer, we can direct you to someone who can. 

You can call free on 0800 032 38 39 or email us at [email protected]

We’re open Monday to Friday (except bank holidays) from 9am-5pm. Outside these hours, you can leave us a message and we’ll get back to you as soon as we can.

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Related content

Lesion (MS lesion)

In MS, the term lesion refers to an area of damage or scarring (sclerosis) in the central nervous system. Lesions are caused by inflammation that results from the immune system attacking the myelin sheath around your nerves.

Central nervous system (CNS)

The nervous system is the network of nerves that allows the body to send messages to and from muscles and organs and to maintain awareness of the outside world through the senses.

Questions about MS?

Call our free helpline on 0800 032 38 39 for practical information you can trust. Or email [email protected]. Available weekdays only.

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“Extra” myelin is responsible for the pathological reaction to mental trauma

Biology

Each oligodendrocyte forms several “legs” that repeatedly “wrap” around a part of an axon, forming a layer of myelin. © Servier Medical Art

: 12.01.2022

Events associated with strong emotional and physical stress and, first of all, life-threatening, usually leave their “trace” in the psyche. Many people develop “post-traumatic stress disorder”; a similar condition has been noted in animals. However, the reaction to traumatic events is highly variable, and now scientists have proposed an explanation for this

Not all people react to severe stress by developing post-traumatic stress disorder (PTSD), and patients with this diagnosis are characterized by a combination of different symptoms. Even genetically identical rats show a range of responses to a stressful situation, from complete ignorance to “avoidant behavior”, the appearance of learning problems or pathological fear. However, the biological basis of these variations is poorly understood.

Nevertheless, back in 2014, American researchers found that in rats after acute stress in the “gray matter” hippocampus (this part of the brain is important for memory formation) more than oligodendrocytes are formed. The outgrowths of these “service” cells of the nervous tissue form the myelin sheath – the same “isolation” covering axons (long processes of neurons) through which nerve impulses pass. Myelin provides a higher speed of transmission of impulses and protects nerve fibers from damage.

Because of the myelin that covers large bundles of axons (long processes of neurons), the inner regions of the brain are called “white matter.” “Gray matter”, in contrast, is mainly the cell bodies of neurons themselves, and their processes in these areas are covered with myelin to a lesser extent

When people talk about problems with myelin, they usually mean a lack of it. Thus, the destruction of myelin occurs in strokes , as well as in multiple sclerosis – a chronic autoimmune disease; myelination disorders often underlie the delays in the physical and mental development of children. But an excess of myelin can also be harmful: due to the too high speed of information transfer between neurons, some nerve circuits become hyperreactive.

Having discovered an increase in the number of myelin-producing cells in rats after stress, scientists suggested that this indicates an increase in myelination in the corresponding parts of the brain. So they recently conducted in-depth studies on lab animals and also analyzed brain MRI scans of 38 U.S. Army veterans, half of whom suffered from PTSD.

To simulate severe mental trauma, 20 experimental rats were immobilized for 3 hours against the background of the smell of a predator (more precisely, fox urine). One week after the experiment, the animals were subjected to behavioral tests, and two weeks later, brain tissue was examined to determine the level of myelination.

As expected, the long-term effects of stress appeared only in some animals. At the same time, they had increased myelination in the areas of the brain responsible for the corresponding pathological symptoms. A similar phenomenon has been found in former military personnel with PTSD. In both humans and rats, avoidance behavior was associated with myelination of the dentate gyrus of the hippocampus, and pathological fear was associated with myelination of the amygdala , which plays a key role in response to strong emotions.

The researchers confirmed these observations in an experiment on rats, in which, using genetic engineering methods, the gene responsible for the synthesis of the olig1 protein was activated in the dentate gyrus of the hippocampus. This protein promotes the formation of mature oligodendrocytes from stem cells, which form the myelin sheath of nerve fibers. As a result, the animals began to show “avoidance behavior” without any stressful exposure – this proves that an increase in the number of these cells in the hippocampus may be associated with the development of anxiety.

True, it is still unclear what is primary and what is secondary here. Either different sensitivity to stress is a consequence of individual differences in the number of oligodendrocytes and the level of myelination, or vice versa. In any case, this knowledge in the future can help identify people who are most vulnerable to stress. This will contribute to the development of a personalized approach in the field of psychiatry, which in this sense lags far behind in comparison with, for example, oncology.

Photo: https://scfh.ru

: 01/12/2022

Myelin – the sheath of neural “wires”

Nerve cells have two types of processes – small and extremely branched dendrites, with which the neuron collects impulses from other nerve cells, and very long axons that send further impulses. Almost all axons in the central nervous system (i.e., in the brain and spinal cord) are covered with myelin, a light-colored substance composed primarily of lipids. There are also many myelinated nerve fibers in the peripheral nervous system, that is, in the nerves that leave the brain and spinal cord and go to other organs.

Oligodendrocyte and myelin sheath. One oligodendrocyte forms a myelin sheath on several axons at once, but on each of them it creates only one sheath segment (from one node of Ranvier to another). Illustration: Holly Fischer/Wikimedia Commons/CC BY 3.0.

Destruction of the myelin sheath in multiple sclerosis. Photo: edesignua/ru.depositphotos. com.

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Myelin simultaneously speeds up the electrochemical impulses traveling through the axons and isolates them from each other, preventing a “short circuit” between neuron “wires”. To understand how myelin speeds up impulses, you need to remember that any impulse in a neuron is a rearrangement of ions between the outer and inner side of the cell membrane. When ion channels open on some part of the membrane, the same ion flows immediately open on the adjacent part of the membrane, then on the part a little further away, etc. The electrical properties of the membrane change sequentially along the neuronal process – this is a running impulse. Myelin wraps the axons in a non-continuous manner from beginning to end. There are gaps in the myelin winding where the membrane is not covered with myelin – the nodes of Ranvier (named after the French physiologist Louis Antoine Ranvier who discovered them). And when the impulse propagates along the axon, the rearrangement of ions occurs just at the nodes of Ranvier. That is, the impulse does not creep slowly between sections that are close to each other, but jumps from one intercept to another. And if in an axon without myelin the impulse runs at a speed of 0.5-10 m/s, then in the same axon, but with myelin, the impulse speed reaches 150 m/s.

Clusters of axons wrapped in myelin appear lighter, so areas in the brain where axon “wires” predominate are called white matter. (Clumps of dendrites that do without myelin form gray matter. Since dendrites are much shorter than axons, they do not transmit impulses over long distances and speed is not so important for them.) Neurons do not produce myelin themselves, there are special cells for this – oligodendrocytes in the central nervous system and Schwann cells in peripheral nerves. Both belong to glia, or neuroglia – this is the name given to the collection of various cells of the nervous system that serve neurons, creating conditions for them to work. Recently, there is more and more evidence that glial cells do not just serve neurons, but directly interfere with their work (see the article “Immune “electricians” of the brain”, “Science and Life” No. 8, 2020). The task of oligodendrocytes and Schwann cells is to make a myelin coil for neurons. An oligodendrocyte or a Schwann cell protrudes its own membrane and wraps around the axon, the membrane grows – and as a result, a layered lipid roll is obtained around the axon. The glial cell remains alive and maintains the integrity of the myelin winding in the part of the axon for which it is responsible.

Destruction of the myelin sheath leads to neurological symptoms of varying types and severity. There are many diseases associated with the loss of myelin on axons, and multiple sclerosis is the most famous among them. This is one of the autoimmune diseases, when the immune system, for some reason, attacks the body’s own cells and molecules. In multiple sclerosis, different immune mechanisms are triggered, which involve both immune cells in the brain and immune cells that have entered the brain from the blood. But, one way or another, everything ends with the fact that the myelin sheath around the axons is destroyed, and sometimes the axons themselves are destroyed.